当前位置： SCI文献检索 > JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY期刊下所有文献 > Class I HDACs regulate angiotensin II-dependent cardiac fibrosis via fibroblasts and circulating fibrocytes.

Class I HDACs regulate angiotensin II-dependent cardiac fibrosis via fibroblasts and circulating fibrocytes.

Abstract：

:Fibrosis, which is defined as excessive accumulation of fibrous connective tissue, contributes to the pathogenesis of numerous diseases involving diverse organ systems. Cardiac fibrosis predisposes individuals to myocardial ischemia, arrhythmias and sudden death, and is commonly associated with diastolic dysfunction. Histone deacetylase (HDAC) inhibitors block cardiac fibrosis in pre-clinical models of heart failure. However, which HDAC isoforms govern cardiac fibrosis, and the mechanisms by which they do so, remains unclear. Here, we show that selective inhibition of class I HDACs potently suppresses angiotensin II (Ang II)-mediated cardiac fibrosis by targeting two key effector cell populations, cardiac fibroblasts and bone marrow-derived fibrocytes. Class I HDAC inhibition blocks cardiac fibroblast cell cycle progression through derepression of the genes encoding the cyclin-dependent kinase (CDK) inhibitors, p15 and p57. In contrast, class I HDAC inhibitors block agonist-dependent differentiation of fibrocytes through a mechanism involving repression of ERK1/2 signaling. These findings define novel roles for class I HDACs in the control of pathological cardiac fibrosis. Furthermore, since fibrocytes have been implicated in the pathogenesis of a variety of human diseases, including heart, lung and kidney failure, our results suggest broad utility for isoform-selective HDAC inhibitors as anti-fibrotic agents that function, in part, by targeting these circulating mesenchymal cells.

journal_name

J Mol Cell Cardiol

journal_title

Journal of molecular and cellular cardiology

authors

Williams SM,Golden-Mason L,Ferguson BS,Schuetze KB,Cavasin MA,Demos-Davies K,Yeager ME,Stenmark KR,McKinsey TA

doi

10.1016/j.yjmcc.2013.12.013

subject

Has Abstract

pub_date

2014-02-01 00:00:00

pages

112-25

eissn

0022-2828

issn

1095-8584

pii

S0022-2828(13)00362-3

journal_volume

67

pub_type

杂志文章

相关文献

JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY文献大全
  • Impaired Ca2+ cycling of nonischemic myocytes contributes to sarcomere dysfunction early after myocardial infarction.

    abstract：:Changes in the nonischemic remote myocardium of the heart contribute to left ventricular dysfunction after ischemia and reperfusion (I/R). Understanding the underlying mechanisms early after I/R is crucial to improve the adaptation of the viable myocardium to increased mechanical demands. Here, we investigated the rol...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2018.04.004

    authors： Kronenbitter A,Funk F,Hackert K,Gorreßen S,Glaser D,Boknik P,Poschmann G,Stühler K,Isić M,Krüger M,Schmitt JP

    更新日期：2018-06-01 00:00:00

  • Heat-shock protein 90 modulates cardiac ventricular hypertrophy via activation of MAPK pathway.

    abstract：:The Raf/MAPK/ERK kinase (Mek)/extracellular signal-regulated kinases (Erk) pathway is activated in cardiac hypertrophy after a myocardial infarction. Although heat-shock protein 90 (Hsp90) may regulate the Raf/Mek/Erk signal pathway, the role of Hsp90 in pathophysiological cardiac hypertrophy remains unclear. In this ...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2018.12.010

    authors： Tamura S,Marunouchi T,Tanonaka K

    更新日期：2019-02-01 00:00:00

  • Effect of treatment on ventricular function and troponin I proteolysis in reperfused myocardium.

    abstract：:Effects of ischemia time and treatment interventions upon troponin I (TnI) proteolysis and function of reperfused myocardium were examined in isolated, perfused rabbit hearts. Hearts were randomized to 90 min aerobic perfusion, 15 min low-flow (1 ml/min) ischemia (I) and 60 min reperfusion (R) or 60 min low-flow I and...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1006/jmcc.2002.1522

    authors： Prasan AM,McCarron HC,Hambly BD,Fermanis GG,Sullivan DR,Jeremy RW

    更新日期：2002-04-01 00:00:00

  • Enrichment of G protein alpha-subunit mRNAS in the AV-conducting system of the mammalian heart.

    abstract：:We investigated the expression pattern of the heterotrimeric G proteins Gs alpha, Gi alpha-2 and Go alpha in rat and guinea-pig heart by in situ hybridization. Cryosections were hybridized with single-stranded 35S-cRNA probes complementary to subtype-specific sequences of the respective mRNAs. Hybridization signals we...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/s0022-2828(95)91659-8

    authors： Eschenhagen T,Laufs U,Schmitz W,Scholz H,Warnholtz A,Weil J,Schäfer HJ

    更新日期：1995-10-01 00:00:00

  • A biochemical method for the quantitation of myocardial scarring after experimental coronary artery occlusion.

    abstract：:The histologic examination and planimetric evaluation of tissue slices has been so far the only available technique for studying the extent of experimental myocardial infarcts in long-term studies; however, this approach is rather time-consuming when the sample size is large. This study describes a new biochemical met...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/s0022-2828(86)80410-2

    authors： Chiariello M,Ambrosio G,Cappelli-Bigazzi M,Perrone-Filardi P,Brigante F,Sifola C

    更新日期：1986-03-01 00:00:00

  • Generation of Fabry cardiomyopathy model for drug screening using induced pluripotent stem cell-derived cardiomyocytes from a female Fabry patient.

    abstract：BACKGROUND:Fabry disease is an X-linked disease caused by mutations in α-galactosidase A (GLA); these mutations result in the accumulation of its substrates, mainly globotriaosylceramide (Gb3). The accumulation of glycosphingolipids induces pathogenic changes in various organs, including the heart, and Fabry cardiomyop...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2018.07.246

    authors： Kuramoto Y,Naito AT,Tojo H,Sakai T,Ito M,Shibamoto M,Nakagawa A,Higo T,Okada K,Yamaguchi T,Lee JK,Miyagawa S,Sawa Y,Sakata Y,Komuro I

    更新日期：2018-08-01 00:00:00

  • Redox regulation of cardiac hypertrophy.

    abstract：:It is increasingly evident that redox-dependent modifications in cellular proteins and signaling pathways (or redox signaling) play important roles in many aspects of cardiac hypertrophy. Indeed, these redox modifications may be intricately linked with the process of hypertrophy wherein there is not only a significant...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章,评审

    doi：10.1016/j.yjmcc.2014.02.002

    authors： Sag CM,Santos CX,Shah AM

    更新日期：2014-08-01 00:00:00

  • Targeting endothelial and myocardial dysfunction with tetrahydrobiopterin.

    abstract：:Tetrahydrobiopterin (BH(4)) is an essential cofactor for aromatic amino acid hydroxylases and for all three nitric oxide synthase (NOS) isoforms. It also has a protective role in the cell as an antioxidant and scavenger of reactive nitrogen and oxygen species. Experimental studies in humans and animals demonstrate tha...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章,评审

    doi：10.1016/j.yjmcc.2011.03.009

    authors： Moens AL,Kietadisorn R,Lin JY,Kass D

    更新日期：2011-10-01 00:00:00

  • Heterotypic docking compatibility of human connexin37 with other vascular connexins.

    abstract：:Human vascular connexins (Cx37, Cx40, Cx43, and Cx45) can form various types of gap junction channels to synchronize vasodilation/constriction to control local circulation. Most of our knowledge on heterotypic gap junctions of these vascular connexins was from studies on rodent connexins. In human vasculature, the sam...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2018.12.013

    authors： Kim NK,Santos-Miranda A,Chen H,Aoyama H,Bai D

    更新日期：2019-02-01 00:00:00

  • Attenuation of myocardial ischaemic injury 24 h after diacylglycerol treatment in vivo.

    abstract：:Previous work suggests that delayed protection against infarction following ischaemic preconditioning of rabbit myocardium may involve the activation of protein kinase C (PKC). Preconditioning in the presence of chelerythrine, an inhibitor of PKC, abolished the late anti-infarct effect of preconditioning. In the studi...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1006/jmcc.1997.0436

    authors： Baxter GF,Mocanu MM,Yellon DM

    更新日期：1997-07-01 00:00:00

  • PICOT is a critical regulator of cardiac hypertrophy and cardiomyocyte contractility.

    abstract：:PICOT (PKC-interacting cousin of thioredoxin) was previously shown to inhibit the development of cardiac hypertrophy, concomitant with an increase in cardiomyocyte contractility. To explore the physiological function of PICOT in the hearts, we generated a PICOT-deficient mouse line by using a gene trap approach. PICOT...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2008.09.124

    authors： Cha H,Kim JM,Oh JG,Jeong MH,Park CS,Park J,Jeong HJ,Park BK,Lee YH,Jeong D,Yang DK,Bernecker OY,Kim DH,Hajjar RJ,Park WJ

    更新日期：2008-12-01 00:00:00

  • NOR-1 modulates the inflammatory response of vascular smooth muscle cells by preventing NFκB activation.

    abstract：:Recent work has highlighted the role of NR4A receptors in atherosclerosis and inflammation. In vascular smooth muscle cell (VSMC) proliferation, however, NOR-1 (neuron-derived orphan receptor-1) exerts antagonistic effects to Nur77 and Nurr1. The aim of this study was to analyse the effect of NOR-1 in VSMC inflammator...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2014.12.015

    authors： Calvayrac O,Rodríguez-Calvo R,Martí-Pamies I,Alonso J,Ferrán B,Aguiló S,Crespo J,Rodríguez-Sinovas A,Rodríguez C,Martínez-González J

    更新日期：2015-03-01 00:00:00

  • Beta-adrenergic receptor blockade modulates Bcl-X(S) expression and reduces apoptosis in failing myocardium.

    abstract：:The mechanisms by which beta-adrenergic receptor (beta-AR) blockade modulates apoptosis in heart failure (HF) are unclear. We examined the impact of beta-AR blockade with metoprolol on myocardial remodeling, apoptosis, pro-apoptotic (Fas, Fas ligand, Bax, and Bcl-X(S)) and anti-apoptotic (Bcl-X(L)and Bcl-2) gene expre...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/s0022-2828(03)00052-x

    authors： Prabhu SD,Wang G,Luo J,Gu Y,Ping P,Chandrasekar B

    更新日期：2003-05-01 00:00:00

  • Molecular mechanisms in H2O2-induced increase in AT1 receptor gene expression in cardiac fibroblasts: A role for endogenously generated Angiotensin II.

    abstract：:The AT1 receptor (AT1R) mediates the manifold actions of angiotensin II in the cardiovascular system. This study probed the molecular mechanisms that link altered redox status to AT1R expression in cardiac fibroblasts. Real-time PCR and western blot analysis showed that H2O2 enhances AT1R mRNA and protein expression v...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2016.05.010

    authors： Anupama V,George M,Dhanesh SB,Chandran A,James J,Shivakumar K

    更新日期：2016-08-01 00:00:00

  • Formation of binucleated cardiac myocytes in rat heart: I. Role of actin-myosin contractile ring.

    abstract：:Cardiac myocytes in rat hearts lose their ability to undergo cytokinesis between day 3 and day 4, resulting in the formation of binucleated myocytes. Failure in the formation of the actin-myosin contractile ring could cause cardiac myocytes to be defective in cytokinesis. Enzymatically isolated cardiac myocytes from 2...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1006/jmcc.1997.0381

    authors： Li F,Wang X,Bunger PC,Gerdes AM

    更新日期：1997-06-01 00:00:00

  • Arrhythmogenic coupling between the Na+ -Ca2+ exchanger and inositol 1,4,5-triphosphate receptor in rat pulmonary vein cardiomyocytes.

    abstract：:Atrial fibrillation, the most common sustained arrhythmia, is believed to be triggered by ectopic electrical activity originating in the myocardial sleeves surrounding the pulmonary veins (PVs). It has been reported that myocardial sleeves have the potential to generate automaticity in response to norepinephrine. This...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2012.01.007

    authors： Okamoto Y,Takano M,Ohba T,Ono K

    更新日期：2012-05-01 00:00:00

  • Influence of action potential duration and resting potential on effects of quinidine, lidocaine and ethmozin on Vmax in guinea-pig papillary muscles.

    abstract：:The effects of class I antiarrhythmic drugs (quinidine, lidocaine, ethmozin) on the maximum upstroke velocity (Vmax) of the action potential (AP) of guinea-pig papillary muscles were investigated in the presence and absence of nifedipine and a potassium-free solution. Nifedipine (10 microM) decreased AP duration from ...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/0022-2828(91)90029-l

    authors： Jurevicius J,Muckus K,Macianskiene R,Chmel-Dunaj GN

    更新日期：1991-02-01 00:00:00

  • Effects of hemodynamic variables on myocardial K+ balance during and after shortlasting ischemia.

    abstract：:Ischemia-induced myocardial potassium loss and post-ischemic potassium reuptake was quantitated in 8 open chest pigs during control conditions and during hemodynamic alterations which have been shown to increase steady state sarcolemmal potassium fluxes. Myocardial K+ balance was continuously computed before, during a...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/0022-2828(89)90673-1

    authors： Aksnes G,Ellingsen O,Rutlen DL,Ilebekk A

    更新日期：1989-12-01 00:00:00

  • Interaction between propranolol and calcium channel blockers in cardiac and vascular smooth muscle.

    abstract：:The ability of the beta-receptor antagonist propranolol to influence the response of isolated cardiac and vascular smooth muscle to several classes of calcium channel blockers was examined. For comparison, the interactions between propranolol and other classes of negative inotropic and vasorelaxant agents was also eva...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/s0022-2828(88)80144-5

    authors： Weishaar RE,Quade MM,Pugsley TA,Shih YH,Taylor DG Jr

    更新日期：1988-10-01 00:00:00

  • Adaptational response in transcription factors during development of myocardial hypertrophy.

    abstract：:Cardiac hypertrophy is characterized, among others, by the molecular events which selectively activate the expression of genes for contractile proteins within individual myocardial cells. As such, myosin light chain 2 (MLC-2), which is upregulated in the hypertrophic state in both rat and human, serves as a marker for...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/s0022-2828(95)92019-6

    authors： Doud SK,Pan LX,Carleton S,Marmorstein S,Siddiqui MA

    更新日期：1995-10-01 00:00:00

  • Immune-inflammatory dysregulation modulates the incidence of progressive fibrosis and diastolic stiffness in the aging heart.

    abstract：:Diastolic dysfunction in the aging heart is a grave condition that challenges the life and lifestyle of a growing segment of our population. This report seeks to examine the role and interrelationship of inflammatory dysregulation in interstitial myocardial fibrosis and progressive diastolic dysfunction in aging mice....

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2010.10.019

    authors： Cieslik KA,Taffet GE,Carlson S,Hermosillo J,Trial J,Entman ML

    更新日期：2011-01-01 00:00:00

  • MitoPlex: A targeted multiple reaction monitoring assay for quantification of a curated set of mitochondrial proteins.

    abstract：:Mitochondria are the major source of cellular energy (ATP), as well as critical mediators of widespread functions such as cellular redox balance, apoptosis, and metabolic flux. The organelles play an especially important role in the maintenance of cardiac homeostasis; their inability to generate ATP following impairme...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2020.03.011

    authors： Stotland AB,Spivia W,Orosco A,Andres AM,Gottlieb RA,Van Eyk JE,Parker SJ

    更新日期：2020-05-01 00:00:00

  • Regulation of the human tumor necrosis factor-alpha promoter by angiotensin II and lipopolysaccharide in cardiac fibroblasts: different cis-acting promoter sequences and transcriptional factors.

    abstract：:We recently showed that angiotensin (ANG) II as well as mechanical stretch stimulated production of tumor necrosis factor (TNF) in cardiac fibroblasts. Presently, we examined the molecular mechanisms by which ANGII and lipopolysaccharide (LPS) upregulate TNF-alpha gene expression. In neonatal rat cardiac fibroblasts, ...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/s0022-2828(03)00210-4

    authors： Sato H,Watanabe A,Tanaka T,Koitabashi N,Arai M,Kurabayashi M,Yokoyama T

    更新日期：2003-10-01 00:00:00

  • Cardiomyocyte cell cycling, maturation, and growth by multinucleation in postnatal swine.

    abstract：BACKGROUND:Rodent cardiomyocytes (CM) undergo mitotic arrest and decline of mononucleated-diploid population post-birth, which are implicated in neonatal loss of heart regenerative potential. However, the dynamics of postnatal CM maturation are largely unknown in swine, despite a similar neonatal cardiac regenerative c...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2020.07.004

    authors： Velayutham N,Alfieri CM,Agnew EJ,Riggs KW,Baker RS,Ponny SR,Zafar F,Yutzey KE

    更新日期：2020-09-01 00:00:00

  • Comparison between the effects of 2-3 butanedione monoxime (BDM) and calcium chloride on myocardial oxygen consumption.

    abstract：:The agent 2,3-butanedione monoxime (BDM) has been reported to reduce the sensitivity of myofilament force development to calcium ions, without affecting the calcium transient in myocardium. One would predict, therefore, that BDM should reduce the contractile state of the heart without reducing the amount of oxygen tha...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/0022-2828(92)91093-k

    authors： de Tombe PP,Burkhoff D,Hunter WC

    更新日期：1992-08-01 00:00:00

  • Stable high level expression of a transfected human HSP70 gene protects a heart-derived muscle cell line against thermal stress.

    abstract：:Heat shock protein 70 (HSP70) has been shown to play a fundamental role in the induction of thermotolerance in many biological systems. Elevated synthesis of HSP70 in response to diverse stresses such as heat, anoxia, ischaemia, ethanol and heavy metals has been correlated with protection against subsequent more sever...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1006/jmcc.1994.1084

    authors： Heads RJ,Latchman DS,Yellon DM

    更新日期：1994-06-01 00:00:00

  • Novel deletions in MYH7 and MYBPC3 identified in Indian families with familial hypertrophic cardiomyopathy.

    abstract：:Mutations causing familial hypertrophic cardiomyopathy (HCM) have been described in at least 11 genes encoding cardiac sarcomeric proteins. In this study, three previously unknown deletions have been identified in the human cardiac genes coding for beta-myosin heavy chain (MYH7 on chromosome 14) and myosin-binding pro...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/s0022-2828(03)00050-6

    authors： Waldmüller S,Sakthivel S,Saadi AV,Selignow C,Rakesh PG,Golubenko M,Joseph PK,Padmakumar R,Richard P,Schwartz K,Tharakan JM,Rajamanickam C,Vosberg HP

    更新日期：2003-06-01 00:00:00

  • Inhibition of sodium influx and improved preservation of rat hearts during hypothermic ischemia by furosemide and bumetanide: a 23Na- and 31P-NMR study.

    abstract：:The importance of the Na+/K+/Cl- co-transport system of the rat myocardial sarcolemma was studied under hypothermic ischemia by investigating the effect of the co-transport blockers furosemide and bumetanide on the sodium influx into the myocardium. The intracellular Na+ accumulation during hypothermic ischemia was fo...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1006/jmcc.1993.1157

    authors： Rubin Y,Navon G

    更新日期：1993-12-01 00:00:00

  • The external work-pressure time integral relationships and the afterload dependence of Frank-Starling mechanism.

    abstract：:The mechanisms underlying the Frank-Starling Law of the heart are elusive and the prevalent notion suggests that it is afterload independent. However, isolated fiber studies reveal that the afterload determines cardiac function through cross-bridge dependent mechanisms. The study explores the roles of the afterload, i...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2009.05.007

    authors： Sela G,Landesberg A

    更新日期：2009-10-01 00:00:00

  • Effects on recovery during acidosis in cardiac myocytes overexpressing CaMKII.

    abstract：:Recovery of intracellular Ca transients and fractional shortening during late phase acidosis are suggested to be associated with CaMKII-dependent processes of which phospholamban (PLB) phosphorylation may play an important role. To test whether increased expression levels of CaMKII may further enhance recovery, we inv...

    journal_title：Journal of molecular and cellular cardiology

    pub_type： 杂志文章

    doi：10.1016/j.yjmcc.2007.09.008

    authors： Sag CM,Dybkova N,Neef S,Maier LS

    更新日期：2007-12-01 00:00:00