Redox regulation of classⅡHDACs and cardiac hypertrophy-中国期刊网

摘要 Oxidativestressplaysanessentialroleinregulatinggrowthanddeathofcardiacmyocytes.ClassⅡhistonedeacetylases（cⅡ-HDACs）arelocalizedprimarilyinthenucleusinunstimulatedcardiacmyocytesandnegativelyregulatecardiachypertrophybyinteractingwithpro-hypertrophictranscriptionfactors,includingmyocyteenhancerfactor2（MEF2）,calmodulin-bindingtranscriptionactivator（CAMTA）,andnuclearfactoractivatedTcells（NFATs）.NuclearlocalizationofcII-HDACsisregulatednotonlybyphosphorylationbutalsothroughoxidationofconservedcysteineresidues（Agoetal2007）,suggestingthatposttranslationalmodulationplaysanimportantroleinmediatingpathologicalcardiachypertrophyandheartfailure.Inthispresentation,Iwilldiscusshowreactiveoxygenspecies（ROS）areproducedintheheartunderstressandhowROSregulatethesubcellularlocalizationofcII-HDACs,therebycausingpathologicalhypertrophy.TheNADPHoxidasefamilyisagroupoftransmembraneproteinsproducingsuperoxideandhydrogenperoxide.Nox4islocalizedprimarilyinmitochondria,endoplasmicreticulum,andnucleus,whoseexpressionisupregulatedbypressureoverloadandheartfailure.Nox4playsanessentialroleinmediatingincreasesinROSinthefailingheart.IncreasedoxidativestressinducesoxidationofcysteineresidesincⅡ-HDACs,suchasC667andC669inHDAC4,whichinturncausesnuclearexitofcⅡ-HDACs.ThecⅡ-HDACsarefurtherphospho-rylatedbytheHDACkinases,includingCa2+calmodulinkinaseandPKD,leadingtoprolongedcytoplasmiclocalizationofcⅡ-HDACsandconsequentcardiachypertrophy.Thioredoxin1（Trx1）,ananti-oxidant,reducesthecriticalcysteineresiduesincⅡ-HDACs,therebyrestoringthenuclearlocalizationofcⅡ-HDACsandinhibitingpathologicalhypertrophy.DownregulationofNox4enhancesnuclearlocalizationofHDAC4,therebyinhibitingcardiachypertrophy,suggestingthatendogenousNox4mediatesoxidationofHDAC4.Insummary,oxidatives

1Lu Weiwei,Sheng Hongzhuan. Treatment of myocardial hypertrophy in patients with PRKAG2 cardiac syndrome.医药卫生,2021-09.
2. Renal sympathetic denervation reduces left ventricular hypertrophy and improves cardiac function in patients with resistant hypertension.心血管疾病,2012-02.
3朱参战;崔长琮;张全发;薛小临;刘维维;刘引会;徐;琳. A Comparative Study of Acute Hemodynamic Effects of Multi -site Cardiac Pacing in patients with cardiac function NYHA class ⅠtoⅡ without bundle branch block.心血管疾病,2001-02.
4WANG Xinghu;JI Haibo;SHENG Jie. OUTPUT REGULATION PROBLEM FOR A CLASS OF SISO INFINITE DIMENSIONAL SYSTEMS VIA A FINITE DIMENSIONAL DYNAMIC CONTROL.系统科学,2014-06.
5Ahmed Harhash;Prashant Rao;Karl B.Kern. The Role of Cardiac Catheterization after Cardiac Arrest.心血管疾病,2018-09.
6黄俊;王梦洪;肖静;彭景添;郑泽琪;彭小平. The Effects of Singal Protein SMADs on Rat Cardiocyte Hypertrophy.心血管疾病,2005-02.
7Lukas Cipryan. The effect of fitness level on cardiac autonomic regulation, IL-6,total antioxidant capacity, and muscle damage responses to a single bout of high-intensity interval training.体育学,2018-03.
8David E Pontefract Srikanth S lyengar Clifford W Barlow. Prosthetic cardiac valves.内科学,2007-04.
9Li Ke-Bei,Qian Zhi-Yong,Qian Xue-Song,Zhou Yong,Zhu Di-Di,Qiu Yuan-Hao,Wang Yao,Hou Xiao-Feng,Zou Jian-Gang,Sheng Yu-Feng. Cardiac electrical and mechanical synchrony of super-responders to cardiac resynchronization therapy.医药卫生,2020-08.
10Paola Gallinari Stefania Di Marco Phillip Jones Michele Pallaoro Christian Steinkühler. HDACs, histone deacetylation and gene transcription： from molecular biology to cancer therapeutics.细胞生物学,2007-03.

Redox regulation of classⅡHDACs and cardiac hypertrophy

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Redox regulation of classⅡHDACs and cardiac hypertrophy

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