Cardiovascular System - Heart Valve Development - Revision history

Z8600021 at 01:46, 20 March 2018

2018-03-20T01:46:31Z

← Older revision		Revision as of 12:46, 20 March 2018
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			* '''The Trileaflet Mitral Valve'''{{#pmid:29304994\|PMID29304994}} "With the advent of 3-dimensional echocardiography, visualization of the mitral valve has greatly improved. ... We describe the latter entity as a left atrioventricular valve because it never achieves the features of a normal mitral valve. We compare the features of isolated clefts of the mural leaflet of the mitral valve with trifoliate left atrioventricular valve found in the setting of AVSDs with intact septal structures to illustrate the current controversy regarding these conditions. In conclusion, our review suggested the reported trileaflet left atrioventricular valves is likely a misnomer because of a lack of consideration of embryologic development and nomenclature, rather than a greater appreciation and identification of a new distinct disease entity."

	* '''Development and maturation of the fibrous components of the arterial roots in the mouse heart'''{{#pmid:29034473\|PMID29034473}} "The arterial roots are important transitional regions of the heart, connecting the intrapericardial components of the aortic and pulmonary trunks with their ventricular outlets. They house the arterial (semilunar) valves and, in the case of the aorta, are the points of coronary arterial attachment. Moreover, because of the semilunar attachments of the valve leaflets, the arterial roots span the anatomic ventriculo-arterial junction. By virtue of this arrangement, the interleaflet triangles, despite being fibrous, are found on the ventricular aspect of the root and located within the left ventricular cavity. Malformations and diseases of the aortic root are common and serious. ...Using Cre-lox-based lineage tracing technology to label progenitor populations, we show that the SMC and fibrous tissue within the walls of the mature arterial roots share a common origin from the second heart field (SHF) and exclude trans-differentiation of myocardium as a source for the interleaflet triangle fibrous tissues. Moreover, we show that the attachment points of the leaflets to the walls, like the leaflets themselves, are derived from the outflow cushions, having contributions from both SHF-derived endothelial cells and neural crest cells. Our data thus show that the arterial roots in the mouse heart are similar to the features described in the human heart. They provide a framework for understanding complex lesions and diseases affecting the aortic root." [[Mouse Development]]		* '''Development and maturation of the fibrous components of the arterial roots in the mouse heart'''{{#pmid:29034473\|PMID29034473}} "The arterial roots are important transitional regions of the heart, connecting the intrapericardial components of the aortic and pulmonary trunks with their ventricular outlets. They house the arterial (semilunar) valves and, in the case of the aorta, are the points of coronary arterial attachment. Moreover, because of the semilunar attachments of the valve leaflets, the arterial roots span the anatomic ventriculo-arterial junction. By virtue of this arrangement, the interleaflet triangles, despite being fibrous, are found on the ventricular aspect of the root and located within the left ventricular cavity. Malformations and diseases of the aortic root are common and serious. ...Using Cre-lox-based lineage tracing technology to label progenitor populations, we show that the SMC and fibrous tissue within the walls of the mature arterial roots share a common origin from the second heart field (SHF) and exclude trans-differentiation of myocardium as a source for the interleaflet triangle fibrous tissues. Moreover, we show that the attachment points of the leaflets to the walls, like the leaflets themselves, are derived from the outflow cushions, having contributions from both SHF-derived endothelial cells and neural crest cells. Our data thus show that the arterial roots in the mouse heart are similar to the features described in the human heart. They provide a framework for understanding complex lesions and diseases affecting the aortic root." [[Mouse Development]]

Z8600021 at 00:06, 13 March 2018

2018-03-13T00:06:43Z

← Older revision		Revision as of 11:06, 13 March 2018
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	An autosomal dominant single-gene cause of congenital heart disease. Patients also have proportionate short stature, facial abnormalities, and an increased risk of myeloproliferative disease. About half the patients have mutations in PTPN11, encoding the protein tyrosine phosphatase SHP2. A recent study in mice has identified PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.{{#pmid:19251646\|PMID19251646}}		An autosomal dominant single-gene cause of congenital heart disease. Patients also have proportionate short stature, facial abnormalities, and an increased risk of myeloproliferative disease. About half the patients have mutations in PTPN11, encoding the protein tyrosine phosphatase SHP2. A recent study in mice has identified PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.{{#pmid:19251646\|PMID19251646}}

			===Bicuspid Aortic Valve===
			GATA4 and NKX2.5 genes have been identified associated with this disorder.

			A recent genetic screening study of GATA4 in 150 patients with bicuspid aortic valve (BAV){{#pmid:29325903\|PMID29325903}} identified a novel heterozygous GATA4 mutation, p.E147X, was identified in a family with BAV transmitted in an autosomal dominant pattern. The nonsense mutation was absent in 600 control chromosomes. The mutation disrupted the synergistic transcriptional activation between GATA4 and NKX2.5, another transcription factor responsible for BAV.

			* [https://www.omim.org/entry/600576 GATA4] - (8p23.1) transcription factors that control gene expression and differentiation in a variety of cell types. Family of DNA-binding proteins recognize a consensus sequence known as the "GATA" motif, important cis-element in the promoters of many genes.
			* [https://www.omim.org/entry/600584 NKX2-5] - (5q35.1) Homeobox-containing gene expressed only in the heart.

			:'''Links:''' [https://www.omim.org/entry/600576 OMIM - GATA4] \| [https://www.omim.org/entry/600584 OMIM - NKX2.5]

	===Calcific Aortic Valve Disease===		===Calcific Aortic Valve Disease===

Z8600021 at 23:47, 12 March 2018

2018-03-12T23:47:48Z

← Older revision		Revision as of 10:47, 13 March 2018
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			* '''Development and maturation of the fibrous components of the arterial roots in the mouse heart'''{{#pmid:29034473\|PMID29034473}} "The arterial roots are important transitional regions of the heart, connecting the intrapericardial components of the aortic and pulmonary trunks with their ventricular outlets. They house the arterial (semilunar) valves and, in the case of the aorta, are the points of coronary arterial attachment. Moreover, because of the semilunar attachments of the valve leaflets, the arterial roots span the anatomic ventriculo-arterial junction. By virtue of this arrangement, the interleaflet triangles, despite being fibrous, are found on the ventricular aspect of the root and located within the left ventricular cavity. Malformations and diseases of the aortic root are common and serious. ...Using Cre-lox-based lineage tracing technology to label progenitor populations, we show that the SMC and fibrous tissue within the walls of the mature arterial roots share a common origin from the second heart field (SHF) and exclude trans-differentiation of myocardium as a source for the interleaflet triangle fibrous tissues. Moreover, we show that the attachment points of the leaflets to the walls, like the leaflets themselves, are derived from the outflow cushions, having contributions from both SHF-derived endothelial cells and neural crest cells. Our data thus show that the arterial roots in the mouse heart are similar to the features described in the human heart. They provide a framework for understanding complex lesions and diseases affecting the aortic root." [[Mouse Development]]

	* '''Review - Calcific Aortic Valve Disease: a Developmental Biology Perspective'''{{#pmid:29520694\|PMID29520694}} "Calcification of the aortic valve is an active process characterized by calcific nodule formation on the aortic surface leading to a less supple and more stiffened cusp, thereby limiting movement and causing clinical stenosis. The mechanisms underlying these pathogenic changes are largely unknown, but emerging studies have suggested that signaling pathways common to valvulogenesis and bone development play significant roles and include Transforming Growth Factor-β (TGF-β), bone morphogenetic protein (BMP), Wnt, Notch, and Sox9."		* '''Review - Calcific Aortic Valve Disease: a Developmental Biology Perspective'''{{#pmid:29520694\|PMID29520694}} "Calcification of the aortic valve is an active process characterized by calcific nodule formation on the aortic surface leading to a less supple and more stiffened cusp, thereby limiting movement and causing clinical stenosis. The mechanisms underlying these pathogenic changes are largely unknown, but emerging studies have suggested that signaling pathways common to valvulogenesis and bone development play significant roles and include Transforming Growth Factor-β (TGF-β), bone morphogenetic protein (BMP), Wnt, Notch, and Sox9."

	* '''Twist1 directly regulates genes that promote cell proliferation and migration in developing heart valves'''{{#pmid:22242143\|PMID22242143}} "Twist1, a basic helix-loop-helix transcription factor, is expressed in mesenchymal precursor populations during embryogenesis and in metastatic cancer cells. In the developing heart, Twist1 is highly expressed in endocardial cushion (ECC) valve mesenchymal cells and is down regulated during valve differentiation and remodeling. Previous studies demonstrated that Twist1 promotes cell proliferation, migration, and expression of primitive extracellular matrix (ECM) molecules in ECC mesenchymal cells. Furthermore, Twist1 expression is induced in human pediatric and adult diseased heart valves."		* '''Twist1 directly regulates genes that promote cell proliferation and migration in developing heart valves'''{{#pmid:22242143\|PMID22242143}} "Twist1, a basic helix-loop-helix transcription factor, is expressed in mesenchymal precursor populations during embryogenesis and in metastatic cancer cells. In the developing heart, Twist1 is highly expressed in endocardial cushion (ECC) valve mesenchymal cells and is down regulated during valve differentiation and remodeling. Previous studies demonstrated that Twist1 promotes cell proliferation, migration, and expression of primitive extracellular matrix (ECM) molecules in ECC mesenchymal cells. Furthermore, Twist1 expression is induced in human pediatric and adult diseased heart valves." [https://www.omim.org/entry/601622 OMIM - TWIST1]

	* '''Hemodynamic patterning of the avian atrioventricular valve'''{{#pmid:21181939\|PMID21181939}} "In this study, we develop an innovative approach to rigorously quantify the evolving hemodynamic environment of the atrioventricular (AV) canal of avian embryos. Ultrasound generated velocity profiles were imported into Micro-Computed Tomography generated anatomically precise cardiac geometries between Hamburger-Hamilton (HH) stages 17 and 30. Computational fluid dynamic simulations were then conducted and iterated until results mimicked in vivo observations. Blood flow in tubular hearts (HH17) was laminar with parallel streamlines, but strong vortices developed simultaneous with expansion of the cushions and septal walls. For all investigated stages, highest wall shear stresses (WSS) are localized to AV canal valve-forming regions. Peak WSS increased from 19.34 dynes/cm(2) at HH17 to 287.18 dynes/cm(2) at HH30, but spatiotemporally averaged WSS became 3.62 dynes/cm(2) for HH17 to 9.11 dynes/cm(2) for HH30. Hemodynamic changes often preceded and correlated with morphological changes~~. These results establish a quantitative baseline supporting future hemodynamic analyses and interpretations~~."		* '''Hemodynamic patterning of the avian atrioventricular valve'''{{#pmid:21181939\|PMID21181939}} "In this study, we develop an innovative approach to rigorously quantify the evolving hemodynamic environment of the atrioventricular (AV) canal of avian embryos. Ultrasound generated velocity profiles were imported into Micro-Computed Tomography generated anatomically precise cardiac geometries between Hamburger-Hamilton (HH) stages 17 and 30. Computational fluid dynamic simulations were then conducted and iterated until results mimicked in vivo observations. Blood flow in tubular hearts (HH17) was laminar with parallel streamlines, but strong vortices developed simultaneous with expansion of the cushions and septal walls. For all investigated stages, highest wall shear stresses (WSS) are localized to AV canal valve-forming regions. Peak WSS increased from 19.34 dynes/cm(2) at HH17 to 287.18 dynes/cm(2) at HH30, but spatiotemporally averaged WSS became 3.62 dynes/cm(2) for HH17 to 9.11 dynes/cm(2) for HH30. Hemodynamic changes often preceded and correlated with morphological changes." [[Chicken Development]]
	\|}		\|}
	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"

Z8600021 at 23:40, 12 March 2018

2018-03-12T23:40:41Z

← Older revision		Revision as of 10:40, 13 March 2018
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	\|}		\|}
	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"
	! More recent papers		! More recent papers
	\|-		\|-
	\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}		\| [[File:Mark_Hill.jpg\|90px\|left]] {{Most_Recent_Refs}}
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	</gallery>		</gallery>
	==Fetal Heart Valve Sounds==		==Fetal Heart Valve Sounds==
	<html5media height="50" width="400">File:Week17 fetal heart rate.mp3</html5media>		{\|
			\| <html5media height="50" width="400">File:Week17 fetal heart rate.mp3</html5media>

	~~Audio recording of the [[Timeline_human_development#Second_Trimester\|Second Trimester]] fetal heart (GA week 17).~~

	The characteristic "lub-dup" sounds are associated with closing of heart valves.		Audio recording of the [[Timeline_human_development#Second_Trimester\|Second Trimester]] fetal heart ({{GA}} week 17).

			\| The characteristic "lub-dup" sounds are associated with closing of heart valves.
	* '''First sound''' (lub) occurs as atrioventricular valves close and signifies beginning of systole (contraction)		* '''First sound''' (lub) occurs as atrioventricular valves close and signifies beginning of systole (contraction)
	* '''Second sound''' (dup) occurs when semilunar valves close at the beginning of ventricular diastole (relaxation)		* '''Second sound''' (dup) occurs when semilunar valves close at the beginning of ventricular diastole (relaxation)

	:Links: [[Fetal Heart Sounds Audio]]		:'''Links:''' [[Fetal Heart Sounds Audio]]
			\|}

	==Molecular==		==Molecular==
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	Tbx5		Tbx5

			{{Factor Links}}

			==Abnormalities==

			===Noonan syndrome===

			An autosomal dominant single-gene cause of congenital heart disease. Patients also have proportionate short stature, facial abnormalities, and an increased risk of myeloproliferative disease. About half the patients have mutations in PTPN11, encoding the protein tyrosine phosphatase SHP2. A recent study in mice has identified PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.{{#pmid:19251646\|PMID19251646}}

			===Calcific Aortic Valve Disease===
			Calcification of the aortic valve shows calcific nodule formation on the aortic surface, leading to a less supple and more stiffened cusp, limiting movement and causing clinical stenosis.{{#pmid:29520694\|PMID29520694}}

			Pathogenic mechanism is unknown but may involve signaling pathways common to valvulogenesis and bone development:
			* Transforming Growth Factor-β (TGF-β)
			* bone morphogenetic protein (BMP)
			* Wnt
			* Notch
			* Sox9


			{{Factor Links}}
	==Images==		==Images==

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	{{Ref-Odgers1939}}		{{Ref-Odgers1939}}


	<gallery>		<gallery>
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	</gallery>		</gallery>

	~~==Abnormalities==~~

	~~===Noonan syndrome===~~

	An autosomal dominant single-gene cause of congenital heart disease. Patients also have proportionate short stature, facial abnormalities, and an increased risk of myeloproliferative disease. About half the patients have mutations in PTPN11, encoding the protein tyrosine phosphatase SHP2. A recent study in mice has identified PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.{{#pmid:19251646\|PMID19251646}}

	~~===Calcific Aortic Valve Disease===~~
	Calcification of the aortic valve shows calcific nodule formation on the aortic surface, leading to a less supple and more stiffened cusp, limiting movement and causing clinical stenosis.{{#pmid:29520694\|PMID29520694}}

	~~Pathogenic mechanism is unknown but may involve signaling pathways common to valvulogenesis and bone development:~~
	* Transforming Growth Factor-β (TGF-β)
	* bone morphogenetic protein (BMP)
	* Wnt
	* Notch
	* Sox9


	~~{{Factor Links}}~~
	==References==		==References==
	<references/>		<references/>
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	==External Links==		==External Links==
	{{External Links}}		{{External Links}}

Z8600021 at 23:38, 12 March 2018

2018-03-12T23:38:27Z

← Older revision		Revision as of 10:38, 13 March 2018
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	</gallery>		</gallery>
	==Fetal Heart Valve Sounds==		==Fetal Heart Valve Sounds==
			<html5media height="50" width="400">File:Week17 fetal heart rate.mp3</html5media>
	<~~mp3player~~>File:Week17 fetal heart rate.mp3</~~mp3player~~>

	Audio recording of the [[Timeline_human_development#Second_Trimester\|Second Trimester]] fetal heart (GA week 17).		Audio recording of the [[Timeline_human_development#Second_Trimester\|Second Trimester]] fetal heart (GA week 17).

Z8600021 at 23:36, 12 March 2018

2018-03-12T23:36:56Z

← Older revision		Revision as of 10:36, 13 March 2018
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	* Sox9		* Sox9

	~~{{Factors}}~~

			{{Factor Links}}
	==References==		==References==
	<references/>		<references/>

Z8600021 at 23:28, 12 March 2018

2018-03-12T23:28:44Z

← Older revision		Revision as of 10:28, 13 March 2018
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	The heart valves form between the atria and ventricles (mitral valve, tricuspid valve) and between the atria and blood vessels (aortic valve, pulmonary valve). The cardiac cushions in the atrioventricular (AV) canal contain cells that are the primordia of the cardiac valves. The atrioventricular valves are attached to papillary muscles by chordae tendineae.		The heart valves form between the atria and ventricles (mitral valve, tricuspid valve) and between the atria and blood vessels (aortic valve, pulmonary valve). The cardiac cushions in the atrioventricular (AV) canal contain cells that are the primordia of the cardiac valves. The atrioventricular valves are attached to papillary muscles by chordae tendineae.

	Scleraxis (SCX) is a transcription factor involved in tendon and ligament development and has been identified as also expressed in early heart valve development.~~<ref name=~~PMID24983472~~><pubmed>24983472</pubmed></ref>~~		Scleraxis (SCX) is a transcription factor involved in tendon and ligament development and has been identified as also expressed in early heart valve development.{{#pmid:24983472\|PMID24983472}}

	Mitral valve also called the "bicuspid valve".		Mitral valve also called the "bicuspid valve".
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	* '''Twist1 directly regulates genes that promote cell proliferation and migration in developing heart valves'''~~<ref><pubmed>~~22242143~~</pubmed></ref>~~ "Twist1, a basic helix-loop-helix transcription factor, is expressed in mesenchymal precursor populations during embryogenesis and in metastatic cancer cells. In the developing heart, Twist1 is highly expressed in endocardial cushion (ECC) valve mesenchymal cells and is down regulated during valve differentiation and remodeling. Previous studies demonstrated that Twist1 promotes cell proliferation, migration, and expression of primitive extracellular matrix (ECM) molecules in ECC mesenchymal cells. Furthermore, Twist1 expression is induced in human pediatric and adult diseased heart valves."		* '''Review - Calcific Aortic Valve Disease: a Developmental Biology Perspective'''{{#pmid:29520694\|PMID29520694}} "Calcification of the aortic valve is an active process characterized by calcific nodule formation on the aortic surface leading to a less supple and more stiffened cusp, thereby limiting movement and causing clinical stenosis. The mechanisms underlying these pathogenic changes are largely unknown, but emerging studies have suggested that signaling pathways common to valvulogenesis and bone development play significant roles and include Transforming Growth Factor-β (TGF-β), bone morphogenetic protein (BMP), Wnt, Notch, and Sox9."
	* '''Hemodynamic patterning of the avian atrioventricular valve''' ~~<ref><pubmed>~~21181939~~</pubmed></ref>~~ "In this study, we develop an innovative approach to rigorously quantify the evolving hemodynamic environment of the atrioventricular (AV) canal of avian embryos. Ultrasound generated velocity profiles were imported into Micro-Computed Tomography generated anatomically precise cardiac geometries between Hamburger-Hamilton (HH) stages 17 and 30. Computational fluid dynamic simulations were then conducted and iterated until results mimicked in vivo observations. Blood flow in tubular hearts (HH17) was laminar with parallel streamlines, but strong vortices developed simultaneous with expansion of the cushions and septal walls. For all investigated stages, highest wall shear stresses (WSS) are localized to AV canal valve-forming regions. Peak WSS increased from 19.34 dynes/cm(2) at HH17 to 287.18 dynes/cm(2) at HH30, but spatiotemporally averaged WSS became 3.62 dynes/cm(2) for HH17 to 9.11 dynes/cm(2) for HH30. Hemodynamic changes often preceded and correlated with morphological changes. These results establish a quantitative baseline supporting future hemodynamic analyses and interpretations."
			* '''Twist1 directly regulates genes that promote cell proliferation and migration in developing heart valves'''{{#pmid:22242143\|PMID22242143}} "Twist1, a basic helix-loop-helix transcription factor, is expressed in mesenchymal precursor populations during embryogenesis and in metastatic cancer cells. In the developing heart, Twist1 is highly expressed in endocardial cushion (ECC) valve mesenchymal cells and is down regulated during valve differentiation and remodeling. Previous studies demonstrated that Twist1 promotes cell proliferation, migration, and expression of primitive extracellular matrix (ECM) molecules in ECC mesenchymal cells. Furthermore, Twist1 expression is induced in human pediatric and adult diseased heart valves."

			* '''Hemodynamic patterning of the avian atrioventricular valve'''{{#pmid:21181939\|PMID21181939}} "In this study, we develop an innovative approach to rigorously quantify the evolving hemodynamic environment of the atrioventricular (AV) canal of avian embryos. Ultrasound generated velocity profiles were imported into Micro-Computed Tomography generated anatomically precise cardiac geometries between Hamburger-Hamilton (HH) stages 17 and 30. Computational fluid dynamic simulations were then conducted and iterated until results mimicked in vivo observations. Blood flow in tubular hearts (HH17) was laminar with parallel streamlines, but strong vortices developed simultaneous with expansion of the cushions and septal walls. For all investigated stages, highest wall shear stresses (WSS) are localized to AV canal valve-forming regions. Peak WSS increased from 19.34 dynes/cm(2) at HH17 to 287.18 dynes/cm(2) at HH30, but spatiotemporally averaged WSS became 3.62 dynes/cm(2) for HH17 to 9.11 dynes/cm(2) for HH30. Hemodynamic changes often preceded and correlated with morphological changes. These results establish a quantitative baseline supporting future hemodynamic analyses and interpretations."
	\|}		\|}
	{\| class="wikitable mw-collapsible mw-collapsed"		{\| class="wikitable mw-collapsible mw-collapsed"
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	==Molecular==		==Molecular==

	'''Scleraxis''' (Scx) - basic helix–loop–helix transcription factor expressed in the progenitors and cells of all tendon tissues (mouse).~~<ref><pubmed>~~18802027~~</pubmed></ref>~~		'''Scleraxis''' (Scx) - basic helix–loop–helix transcription factor expressed in the progenitors and cells of all tendon tissues (mouse).{{#pmid:18802027\|PMID18802027}}

	'''Periostin''' - regulates lineage commitment of valve precursor cells (chicken).~~<ref><pubmed>~~19334280~~</pubmed></ref>~~		'''Periostin''' - regulates lineage commitment of valve precursor cells (chicken).{{#pmid:19334280\|PMID19334280}}

	Gata4 and Gata6		Gata4 and Gata6
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	===Noonan syndrome===		===Noonan syndrome===

	An autosomal dominant single-gene cause of congenital heart disease. Patients also have proportionate short stature, facial abnormalities, and an increased risk of myeloproliferative disease. About half the patients have mutations in PTPN11, encoding the protein tyrosine phosphatase SHP2. A recent study in mice has identified PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.~~<ref><pubmed>~~19251646~~</pubmed></ref>~~		An autosomal dominant single-gene cause of congenital heart disease. Patients also have proportionate short stature, facial abnormalities, and an increased risk of myeloproliferative disease. About half the patients have mutations in PTPN11, encoding the protein tyrosine phosphatase SHP2. A recent study in mice has identified PTPN11 acting in endocardium to enhance endocardial-mesenchymal transformation.{{#pmid:19251646\|PMID19251646}}

			===Calcific Aortic Valve Disease===
			Calcification of the aortic valve shows calcific nodule formation on the aortic surface, leading to a less supple and more stiffened cusp, limiting movement and causing clinical stenosis.{{#pmid:29520694\|PMID29520694}}

			Pathogenic mechanism is unknown but may involve signaling pathways common to valvulogenesis and bone development:
			* Transforming Growth Factor-β (TGF-β)
			* bone morphogenetic protein (BMP)
			* Wnt
			* Notch
			* Sox9

			{{Factors}}

	==References==		==References==
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	===Reviews===		===Reviews===
	~~<pubmed>~~20809794~~</pubmed>~~		{{#pmid:20809794}}
	~~<pubmed>~~20201901~~</pubmed>~~
	~~<pubmed>~~14567955~~</pubmed>~~		{{#pmid:20201901}}
	~~<pubmed>~~12768658~~</pubmed>~~
			{{#pmid:14567955}}

			{{#pmid:12768658}}

	===Articles===		===Articles===
			{{#pmid:17549728}}

			{{#pmid:16914500}}

	~~<pubmed>17549728</pubmed>~~		{{#pmid:17104787}}
	~~<pubmed>16914500</pubmed>~~
	~~<pubmed>~~17104787~~</pubmed>~~

	===Search PubMed===		===Search PubMed===

Z8600021 at 15:10, 1 Haziran 2016

2016-06-01T15:10:05Z

← Older revision		Revision as of 02:10, 2 Haziran 2016
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	===Historic===		===Historic===
	{{Historic Disclaimer}}		{{Historic Disclaimer}}
	~~Odgers PNB. [[Paper~~ - ~~The Development of the Atrio-Ventricular Valves in Man\|The Development of the Atrio-Ventricular Valves in Man]] (1939) J Anat. 73:643-57. PMID 17104787~~
			{{Ref-Odgers1939}}


	<gallery>		<gallery>

Z8600021 at 05:32, 15 November 2015

2015-11-15T05:32:33Z

← Older revision		Revision as of 16:32, 15 November 2015
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	</gallery>		</gallery>

	~~</gallery>~~
	==Abnormalities==		==Abnormalities==

Z8600021 at 05:31, 15 November 2015

2015-11-15T05:31:49Z

← Older revision		Revision as of 16:31, 15 November 2015
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	File:Odgers1939-fig05.jpg\|5 right lateral cusp in a 28.5 mm. embryo		File:Odgers1939-fig05.jpg\|5 right lateral cusp in a 28.5 mm. embryo
	File:Odgers1939-plate02.jpg\|Plate 2		File:Odgers1939-plate02.jpg\|Plate 2
			File:Odgers1939-fig06.jpg\|6 right lateral cusp in a 46 mm. embryo
			File:Odgers1939-fig07.jpg\|7 right lateral cusp in a 61 mm. embryo
			File:Odgers1939-fig08.jpg\|8 right lateral cusp in an 85 mm. foetus
			File:Odgers1939-fig09.jpg\|9 right lateral cusp in a 210 mm. foetus
			File:Odgers1939-fig10.jpg\|right lateral cusp of a full time foetus
			</gallery>

	</gallery>		</gallery>
	==Abnormalities==		==Abnormalities==

← Older revision		Revision as of 10:47, 13 March 2018
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			* '''Development and maturation of the fibrous components of the arterial roots in the mouse heart'''{{#pmid:29034473\|PMID29034473}} "The arterial roots are important transitional regions of the heart, connecting the intrapericardial components of the aortic and pulmonary trunks with their ventricular outlets. They house the arterial (semilunar) valves and, in the case of the aorta, are the points of coronary arterial attachment. Moreover, because of the semilunar attachments of the valve leaflets, the arterial roots span the anatomic ventriculo-arterial junction. By virtue of this arrangement, the interleaflet triangles, despite being fibrous, are found on the ventricular aspect of the root and located within the left ventricular cavity. Malformations and diseases of the aortic root are common and serious. ...Using Cre-lox-based lineage tracing technology to label progenitor populations, we show that the SMC and fibrous tissue within the walls of the mature arterial roots share a common origin from the second heart field (SHF) and exclude trans-differentiation of myocardium as a source for the interleaflet triangle fibrous tissues. Moreover, we show that the attachment points of the leaflets to the walls, like the leaflets themselves, are derived from the outflow cushions, having contributions from both SHF-derived endothelial cells and neural crest cells. Our data thus show that the arterial roots in the mouse heart are similar to the features described in the human heart. They provide a framework for understanding complex lesions and diseases affecting the aortic root." [[Mouse Development]]

	* '''Review - Calcific Aortic Valve Disease: a Developmental Biology Perspective'''{{#pmid:29520694\|PMID29520694}} "Calcification of the aortic valve is an active process characterized by calcific nodule formation on the aortic surface leading to a less supple and more stiffened cusp, thereby limiting movement and causing clinical stenosis. The mechanisms underlying these pathogenic changes are largely unknown, but emerging studies have suggested that signaling pathways common to valvulogenesis and bone development play significant roles and include Transforming Growth Factor-β (TGF-β), bone morphogenetic protein (BMP), Wnt, Notch, and Sox9."		* '''Review - Calcific Aortic Valve Disease: a Developmental Biology Perspective'''{{#pmid:29520694\|PMID29520694}} "Calcification of the aortic valve is an active process characterized by calcific nodule formation on the aortic surface leading to a less supple and more stiffened cusp, thereby limiting movement and causing clinical stenosis. The mechanisms underlying these pathogenic changes are largely unknown, but emerging studies have suggested that signaling pathways common to valvulogenesis and bone development play significant roles and include Transforming Growth Factor-β (TGF-β), bone morphogenetic protein (BMP), Wnt, Notch, and Sox9."

	* '''Twist1 directly regulates genes that promote cell proliferation and migration in developing heart valves'''{{#pmid:22242143\|PMID22242143}} "Twist1, a basic helix-loop-helix transcription factor, is expressed in mesenchymal precursor populations during embryogenesis and in metastatic cancer cells. In the developing heart, Twist1 is highly expressed in endocardial cushion (ECC) valve mesenchymal cells and is down regulated during valve differentiation and remodeling. Previous studies demonstrated that Twist1 promotes cell proliferation, migration, and expression of primitive extracellular matrix (ECM) molecules in ECC mesenchymal cells. Furthermore, Twist1 expression is induced in human pediatric and adult diseased heart valves."		* '''Twist1 directly regulates genes that promote cell proliferation and migration in developing heart valves'''{{#pmid:22242143\|PMID22242143}} "Twist1, a basic helix-loop-helix transcription factor, is expressed in mesenchymal precursor populations during embryogenesis and in metastatic cancer cells. In the developing heart, Twist1 is highly expressed in endocardial cushion (ECC) valve mesenchymal cells and is down regulated during valve differentiation and remodeling. Previous studies demonstrated that Twist1 promotes cell proliferation, migration, and expression of primitive extracellular matrix (ECM) molecules in ECC mesenchymal cells. Furthermore, Twist1 expression is induced in human pediatric and adult diseased heart valves." [https://www.omim.org/entry/601622 OMIM - TWIST1]

	* '''Hemodynamic patterning of the avian atrioventricular valve'''{{#pmid:21181939\|PMID21181939}} "In this study, we develop an innovative approach to rigorously quantify the evolving hemodynamic environment of the atrioventricular (AV) canal of avian embryos. Ultrasound generated velocity profiles were imported into Micro-Computed Tomography generated anatomically precise cardiac geometries between Hamburger-Hamilton (HH) stages 17 and 30. Computational fluid dynamic simulations were then conducted and iterated until results mimicked in vivo observations. Blood flow in tubular hearts (HH17) was laminar with parallel streamlines, but strong vortices developed simultaneous with expansion of the cushions and septal walls. For all investigated stages, highest wall shear stresses (WSS) are localized to AV canal valve-forming regions. Peak WSS increased from 19.34 dynes/cm(2) at HH17 to 287.18 dynes/cm(2) at HH30, but spatiotemporally averaged WSS became 3.62 dynes/cm(2) for HH17 to 9.11 dynes/cm(2) for HH30. Hemodynamic changes often preceded and correlated with morphological changes~~. These results establish a quantitative baseline supporting future hemodynamic analyses and interpretations~~."		* '''Hemodynamic patterning of the avian atrioventricular valve'''{{#pmid:21181939\|PMID21181939}} "In this study, we develop an innovative approach to rigorously quantify the evolving hemodynamic environment of the atrioventricular (AV) canal of avian embryos. Ultrasound generated velocity profiles were imported into Micro-Computed Tomography generated anatomically precise cardiac geometries between Hamburger-Hamilton (HH) stages 17 and 30. Computational fluid dynamic simulations were then conducted and iterated until results mimicked in vivo observations. Blood flow in tubular hearts (HH17) was laminar with parallel streamlines, but strong vortices developed simultaneous with expansion of the cushions and septal walls. For all investigated stages, highest wall shear stresses (WSS) are localized to AV canal valve-forming regions. Peak WSS increased from 19.34 dynes/cm(2) at HH17 to 287.18 dynes/cm(2) at HH30, but spatiotemporally averaged WSS became 3.62 dynes/cm(2) for HH17 to 9.11 dynes/cm(2) for HH30. Hemodynamic changes often preceded and correlated with morphological changes." [[Chicken Development]]
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