About: Cardiac hypertrophy is not a required compensatory response to short-term pressure overload

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About: Cardiac hypertrophy is not a required compensatory response to short-term pressure overload Goto Sponge NotDistinct Permalink

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scientific article published on 01 June 2000

Attributes	Values
rdf:type	Item
description	wetenschappelijk artikel (nl) наукова стаття, опублікована в червні 2000 (uk) im Juni 2000 veröffentlichter wissenschaftlicher Artikel (de) artículu científicu espublizáu en xunu de 2000 (ast) scientific article published on 01 June 2000 (en)
publication date	wds:Q73907450-720879A2-9A30-44F5-AB9F-3908CDE97CFC
publication date	2000-06-01 00:00:00Z (xsd:dateTime)
language of work or name	wds:Q73907450-286076F3-A555-4229-B413-11D5099E26CB
language of work or name	English
author name string	wds:Q73907450-2F45E767-B0DE-4CFC-A94D-A52CE8890924 wds:Q73907450-48626276-8651-4858-B9D2-CDA2081E05A3 wds:Q73907450-4A5A5606-FED1-4CA3-B6EB-F9E0D896870D wds:Q73907450-55A4F47A-81CA-4CDF-82D1-713DF860742B wds:Q73907450-76EFB0BF-3725-45E5-8D90-81F9759ADFEF wds:Q73907450-A3B0C458-E487-4259-9F51-DE410D7642EA wds:Q73907450-CBE1FA9C-155E-4D29-8DB1-BF46D55D9E32 wds:Q73907450-E119FF1B-BB85-4B17-A7C5-D846351DF7CF
author name string	Wang Z Karimi M Kutschke W Weiss RM Zimmerman K Hill JA Kerber RE Davisson RL
rdfs:label	Cardiac hypertrophy is not a required compensatory response to short-term pressure overload (en) Cardiac hypertrophy is not a required compensatory response to short-term pressure overload (nl)
skos:prefLabel	Cardiac hypertrophy is not a required compensatory response to short-term pressure overload (en) Cardiac hypertrophy is not a required compensatory response to short-term pressure overload (nl)
name	Cardiac hypertrophy is not a required compensatory response to short-term pressure overload (en) Cardiac hypertrophy is not a required compensatory response to short-term pressure overload (nl)
title	wds:Q73907450-6790F371-7960-4303-9B35-FDD3CE2F3C35
title	Cardiac hypertrophy is not a required compensatory response to short-term pressure overload (en)
page(s)	wds:Q73907450-EDE808F3-4E5A-4262-A7D5-F1A6B40A09FD
page(s)	2863-2869
instance of	wds:Q73907450-DC7B6BF9-8EBB-450D-9A4D-E2D84C6BD121
instance of	scholarly article
PubMed ID	wds:Q73907450-6C3FC26D-EB95-420D-A374-880A1583DDD0
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/10859294
PubMed ID	10859294
published in	wds:Q73907450-F858B68D-9DF7-4279-BDF7-98D28ECF8709
published in	Circulation
issue	wds:Q73907450-F18FB8F6-5125-40E9-82A4-A685EEF2D568
volume	wds:Q73907450-89F4BDB8-E9B0-4D53-B46E-B2445430459B
issue	24
volume	101
DOI	wds:Q73907450-B6CE3BCE-78E3-4C8E-B216-D72129DA3250
DOI	http://dx.doi.org/10.1161/01.CIR.101.24.2863
DOI	10.1161/01.CIR.101.24.2863
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q73907450
is cites work of	Glucose regulation of load-induced mTOR signaling and ER stress in mammalian heart Reversibility of adverse, calcineurin-dependent cardiac remodeling Suppression of class I and II histone deacetylases blunts pressure-overload cardiac hypertrophy Translational suppression of atrophic regulators by microRNA-23a integrates resistance to skeletal muscle atrophy. Nix-mediated apoptosis links myocardial fibrosis, cardiac remodeling, and hypertrophy decompensation Decoding calcium signals involved in cardiac growth and function Dietary sodium alters the prevalence of electrocardiogram determined left ventricular hypertrophy in hypertension Inhibition of left ventricular remodelling preserves chamber systolic function in pressure-overloaded mice Early echocardiographic predictors of outcomes in the mouse transverse aortic constriction heart failure model Dysferlin-mediated membrane repair protects the heart from stress-induced left ventricular injury What causes a broken heart--molecular insights into heart failure Differential cardiac remodeling in preload versus afterload CaMKII inhibition in heart failure, beneficial, harmful, or both The delta isoform of CaM kinase II is required for pathological cardiac hypertrophy and remodeling after pressure overload CaMKII negatively regulates calcineurin-NFAT signaling in cardiac myocytes Stress-dependent cardiac remodeling occurs in the absence of microRNA-21 in mice Class II histone deacetylases act as signal-responsive repressors of cardiac hypertrophy Targeted disruption of NFATc3, but not NFATc4, reveals an intrinsic defect in calcineurin-mediated cardiac hypertrophic growth The transcriptional coactivator CAMTA2 stimulates cardiac growth by opposing class II histone deacetylases Histone deacetylase (HDAC) inhibitors attenuate cardiac hypertrophy by suppressing autophagy Histone deacetylases 5 and 9 govern responsiveness of the heart to a subset of stress signals and play redundant roles in heart development Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractility The MEF2D transcription factor mediates stress-dependent cardiac remodeling in mice Cardiac autophagy is a maladaptive response to hemodynamic stress Polycystin-1 Is a Cardiomyocyte Mechanosensor That Governs L-Type Ca2+ Channel Protein Stability Activated glycogen synthase-3 beta suppresses cardiac hypertrophy in vivo Myocyte-enriched calcineurin-interacting protein, MCIP1, inhibits cardiac hypertrophy in vivo Transverse aortic constriction leads to accelerated heart failure in mice lacking PPAR-gamma coactivator 1alpha Atrogin-1/muscle atrophy F-box inhibits calcineurin-dependent cardiac hypertrophy by participating in an SCF ubiquitin ligase complex Mice lacking calsarcin-1 are sensitized to calcineurin signaling and show accelerated cardiomyopathy in response to pathological biomechanical stress Modulatory calcineurin-interacting proteins 1 and 2 function as calcineurin facilitators in vivo A knockin mouse model of the Bardet-Biedl syndrome 1 M390R mutation has cilia defects, ventriculomegaly, retinopathy, and obesity Differential activation of stress-response signaling in load-induced cardiac hypertrophy and failure Distinct cellular and molecular mechanisms underlie functional remodeling of repolarizing K+ currents with left ventricular hypertrophy miR-9 and NFATc3 regulate myocardin in cardiac hypertrophy Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice Targeted inhibition of calcineurin attenuates cardiac hypertrophy in vivo Physiological and pathological cardiac hypertrophy. Effects of deep sedation or general anesthesia on cardiac function in mice undergoing cardiovascular magnetic resonance Protein kinase cascades in the regulation of cardiac hypertrophy A signature pattern of stress-responsive microRNAs that can evoke cardiac hypertrophy and heart failure Doppler evaluation of peripheral vascular adaptations to transverse aortic banding in mice TRPC6 fulfills a calcineurin signaling circuit during pathologic cardiac remodeling In vivo suppression of polyglutamine neurotoxicity by C-terminus of Hsp70-interacting protein (CHIP) supports an aggregation model of pathogenesis. Nox2 deficiency prevents hypertension-induced vascular dysfunction and hypertrophy in cerebral arterioles Modulation of adverse cardiac remodeling by STARS, a mediator of MEF2 signaling and SRF activity Abnormal myocardial insulin signalling in type 2 diabetes and left-ventricular dysfunction Foxo transcription factors blunt cardiac hypertrophy by inhibiting calcineurin signaling Glycogen synthase kinase-3beta regulates post-myocardial infarction remodeling and stress-induced cardiomyocyte proliferation in vivo

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