Adolescent feline heart contains a population of small, proliferative ventricular myocytes with immature physiological properties.
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Cellular therapy promotes endogenous stem cell repairInhibition of doxorubicin-induced senescence by PPARδ activation agonists in cardiac muscle cells: cooperation between PPARδ and Bcl6Notch1 signaling stimulates proliferation of immature cardiomyocytesDoxorubicin induces senescence or apoptosis in rat neonatal cardiomyocytes by regulating the expression levels of the telomere binding factors 1 and 2.Bone-derived stem cells repair the heart after myocardial infarction through transdifferentiation and paracrine signaling mechanisms.Association of leukocyte telomere length with echocardiographic left ventricular mass: the Framingham heart studyMagnetic targeting enhances engraftment and functional benefit of iron-labeled cardiosphere-derived cells in myocardial infarction.Site-specific microtubule-associated protein 4 dephosphorylation causes microtubule network densification in pressure overload cardiac hypertrophyDe novo myocardial regeneration: advances and pitfalls.Down-regulation of replication factor C-40 (RFC40) causes chromosomal missegregation in neonatal and hypertrophic adult rat cardiac myocytes.Expansion of human cardiac stem cells in physiological oxygen improves cell production efficiency and potency for myocardial repairAdhesion proteins, stem cells, and arrhythmogenesis.T-type Ca²+ signalling regulates aldosterone-induced CREB activation and cell death through PP2A activation in neonatal cardiomyocytesMouse strain determines cardiac growth potential.MicroRNA induced cardiac reprogramming in vivo: evidence for mature cardiac myocytes and improved cardiac function.GABAergic contributions to alcohol responsivity during adolescence: insights from preclinical and clinical studiesCa2+- and mitochondrial-dependent cardiomyocyte necrosis as a primary mediator of heart failureThe role of neuregulin/ErbB2/ErbB4 signaling in the heart with special focus on effects on cardiomyocyte proliferationCardiomyocyte proliferation contributes to heart growth in young humans.Cardiomyocyte proliferation and progenitor cell recruitment underlie therapeutic regeneration after myocardial infarction in the adult mouse heart.Bioenergetic and functional consequences of cellular therapy: activation of endogenous cardiovascular progenitor cellsGenesis of myocardial repair with cardiac progenitor cells and tissue engineeringCardiomyogenic stem and progenitor cell plasticity and the dissection of cardiopoiesis.Distinct roles of GSK-3alpha and GSK-3beta phosphorylation in the heart under pressure overloadStem cells in the heart: what's the buzz all about? Part 2: Arrhythmic risks and clinical studies.Hypoxic preconditioning enhances the benefit of cardiac progenitor cell therapy for treatment of myocardial infarction by inducing CXCR4 expression.T-type Ca²⁺ channels regulate the exit of cardiac myocytes from the cell cycle after birth.β-myosin heavy chain is induced by pressure overload in a minor subpopulation of smaller mouse cardiac myocytes.Tetrodotoxin-sensitive Ca2+ Currents, but No T-type Currents in Normal, Hypertrophied, and Failing Mouse Cardiomyocytes.Stem cell therapy for ischemic heart disease.Hypoxic Stress Decreases c-Myc Protein Stability in Cardiac Progenitor Cells Inducing Quiescence and Compromising Their Proliferative and Vasculogenic Potential.Do binucleate cardiomyocytes have a role in myocardial repair? Insights using isolated rodent myocytes and cell culture.Repair of the injured adult heart involves new myocytes potentially derived from resident cardiac stem cells.Persistent increases in Ca(2+) influx through Cav1.2 shortens action potential and causes Ca(2+) overload-induced afterdepolarizations and arrhythmias.Imatinib activates pathological hypertrophy by altering myocyte calcium regulation.Cardiospheres recapitulate a niche-like microenvironment rich in stemness and cell-matrix interactions, rationalizing their enhanced functional potency for myocardial repairT-tubule remodeling during transition from hypertrophy to heart failure.Revascularization of chronic hibernating myocardium stimulates myocyte proliferation and partially reverses chronic adaptations to ischemia.Calcium influx through Cav1.2 is a proximal signal for pathological cardiomyocyte hypertrophy.Functional ion channels in mouse cardiac c-kit(+) cells.
P2860
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P2860
Adolescent feline heart contains a population of small, proliferative ventricular myocytes with immature physiological properties.
description
2007 nî lūn-bûn
@nan
2007年の論文
@ja
2007年学术文章
@wuu
2007年学术文章
@zh
2007年学术文章
@zh-cn
2007年学术文章
@zh-hans
2007年学术文章
@zh-my
2007年学术文章
@zh-sg
2007年學術文章
@yue
2007年學術文章
@zh-hant
name
Adolescent feline heart contai ...... ture physiological properties.
@en
Adolescent feline heart contai ...... ture physiological properties.
@nl
type
label
Adolescent feline heart contai ...... ture physiological properties.
@en
Adolescent feline heart contai ...... ture physiological properties.
@nl
prefLabel
Adolescent feline heart contai ...... ture physiological properties.
@en
Adolescent feline heart contai ...... ture physiological properties.
@nl
P2093
P50
P1433
P1476
Adolescent feline heart contai ...... ture physiological properties.
@en
P2093
Annarosa Leri
Claudia Bearzi
David M Harris
Federico Mosna
Hajime Kubo
Irina Trofimova
Jan Kajstura
Jochen Tillmanns
Leanne Cribbs
Naser Jaleel
P304
P356
10.1161/01.RES.0000259560.39234.99
P577
2007-02-01T00:00:00Z