{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,20]],"date-time":"2026-08-20T14:52:07Z","timestamp":1787237527340,"version":"build-2736575974"},"reference-count":45,"publisher":"Bentham Science Publishers Ltd.","issue":"4","license":[{"start":{"date-parts":[[2023,3,30]],"date-time":"2023-03-30T00:00:00Z","timestamp":1680134400000},"content-version":"vor","delay-in-days":29,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/legalcode"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82070231"],"award-info":[{"award-number":["82070231"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100012166","name":"National Key R&D Program of China","doi-asserted-by":"publisher","award":["2022YFA1104500"],"award-info":[{"award-number":["2022YFA1104500"]}],"id":[{"id":"10.13039\/501100012166","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100017607","name":"Shenzhen Fundamental Research Program","doi-asserted-by":"publisher","award":["ZDSYS 20200923172 000001"],"award-info":[{"award-number":["ZDSYS 20200923172 000001"]}],"id":[{"id":"10.13039\/501100017607","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100010877","name":"Shenzhen Science and Technology Innovation Commission","doi-asserted-by":"publisher","award":["RCJC20210706091947009"],"award-info":[{"award-number":["RCJC20210706091947009"]}],"id":[{"id":"10.13039\/501100010877","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100021171","name":"Guangdong Basic and Applied Basic Research Foundation","doi-asserted-by":"publisher","award":["2022A1515012517"],"award-info":[{"award-number":["2022A1515012517"]}],"id":[{"id":"10.13039\/501100021171","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["eurekaselect.com"],"crossmark-restriction":true},"short-container-title":["CDT"],"published-print":{"date-parts":[[2023,3]]},"abstract":"<jats:sec>\n                    <jats:title>aims:<\/jats:title>\n                    <jats:p>To elucidate the roles of PRC2 and HDACs in cardiomyocyte hypertrophy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>background:<\/jats:title>\n                    <jats:p>Postnatal cardiomyocytes respond to stress signals by hypertrophic growth and fetal gene reprogramming, which involves epigenetic remodeling mediated by histone methyltransferase polycomb repressive complex 2 (PRC2) and histone deacetylases (HDACs).  However, it remains unclear to what extent these histone modifiers contribute to the development of cardiomyocyte hypertrophy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>objective:<\/jats:title>\n                    <jats:p>To compare the dose-dependent effects of GSK126 and TSA, inhibitors of PRC2 and HDACs, respectively, on cardiomyocyte hypertrophy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>method:<\/jats:title>\n                    <jats:p>Neonatal rat ventricular myocytes (NRVMs) were stimulated by phenylephrine (PE; 50\u03bcM) to induce hypertrophy in the presence or absence of the PRC2 inhibitor GSK126 or the HDACs inhibitor Trichostatin A (TSA). Histone methylation and acetylation were measured by Western blot. Cell size was determined by wheat germ agglutinin (WGA) staining. Cardiac hypertrophy markers were quantified by quantitative reverse transcription polymerase chain reaction (qRT-PCR).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>result:<\/jats:title>\n                    <jats:p>PE treatment induced the expression of cardiac hypertrophy markers, including natriuretic peptide A (Nppa), natriuretic peptide B (Nppb),  and myosin heavy chain 7 (Myh7), in a time-dependent manner in NRVMs. Histone modifications, including H3K27me3, H3K9ac, and H3K27ac, were dynamically altered after PE treatment. Treatment with TSA and GSK126 dose-dependently repressed histone acetylation and methylation, respectively. Whereas TSA reversed the PE-induced cell size enlargement in a wide range of concentrations, cardiomyocyte hypertrophy was only inhibited by GSK126 at a higher dose (1\u03bcM). Consistently, TSA dose-dependently suppressed the induction of Nppa, Nppb, and Myh7\/Myh6 ratio, while these indexes were only inhibited by GSK126 at 1\u03bcM. However, TSA, but not GSK126, caused pro-hypertrophic expression of pathological genes at the basal level.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>conclusion:<\/jats:title>\n                    <jats:p>Our data demonstrate diversified effects of TSA and GSK126 on PE-induced cardiomyocyte hypertrophy, and shed a light on the epigenetic reprogramming in the pathogenesis of cardiac hypertrophy.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>other:<\/jats:title>\n                    <jats:p>Our data systematically compared the effects of TSA and GSK126 on PE-induced cardiomyocyte hypertrophy, and demonstrate the concentration thresholds for their protective function.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2174\/1389450124666230124094936","type":"journal-article","created":{"date-parts":[[2023,2,3]],"date-time":"2023-02-03T10:14:31Z","timestamp":1675419271000},"page":"371-378","update-policy":"https:\/\/doi.org\/10.2174\/bsp_crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Dose-dependent Effects of PRC2 and HDAC Inhibitors on Cardiomyocyte\nHypertrophy Induced by Phenylephrine"],"prefix":"10.2174","volume":"24","author":[{"given":"Weixin","family":"Chen","sequence":"first","affiliation":[{"name":"Department of Cardiology, Fuwai Hospital Chinese\nAcademy of Medical Sciences, Shenzhen, 518057, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhihua","family":"Wang","sequence":"first","affiliation":[{"name":"2Shenzhen Key Laboratory\nof Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, 518057, China"},{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease,\nChinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhenyi","family":"Zhao","sequence":"additional","affiliation":[{"name":"School of Pharmacy, Health Science Center, Shenzhen University, Shenzhen 518060, China"},{"name":"Shenzhen Key Laboratory\nof Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, 518057, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jian","family":"Lv","sequence":"additional","affiliation":[{"name":"Shenzhen Key Laboratory\nof Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, 518057, China"},{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease,\nChinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China"},{"name":"Department\nof Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ningning","family":"Guo","sequence":"additional","affiliation":[{"name":"Shenzhen Key Laboratory\nof Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, 518057, China"},{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease,\nChinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiuxiao","family":"Guo","sequence":"additional","affiliation":[{"name":"Shenzhen Key Laboratory\nof Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, 518057, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sai","family":"Zeng","sequence":"additional","affiliation":[{"name":"Shenzhen Key Laboratory\nof Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, 518057, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yu","family":"Fang","sequence":"additional","affiliation":[{"name":"Shenzhen Key Laboratory\nof Cardiovascular Disease, Fuwai Hospital Chinese Academy of Medical Sciences, Shenzhen, 518057, China"},{"name":"State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Disease,\nChinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100037, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"965","reference":[{"key":"ref=1","doi-asserted-by":"publisher","first-page":"387","DOI":"10.1038\/s41569-018-0007-y","volume":"15","author":"Nakamura M.","year":"2018","unstructured":"Nakamura M.; Sadoshima J.; Mechanisms of physiological and pathological cardiac hypertrophy. Nat Rev Cardiol 2018,15(7),387-407","journal-title":"Nat Rev Cardiol"},{"key":"ref=2","doi-asserted-by":"publisher","first-page":"1224","DOI":"10.1093\/eurheartj\/ehn156","volume":"29","author":"MacDonald M.R.","year":"2008","unstructured":"MacDonald M.R.; Petrie M.C.; Hawkins N.M.; Petrie J.R.; Fisher M.; McKelvie R.; Aguilar D.; Krum H.; McMurray J.J.V.; Diabetes, left ventricular systolic dysfunction, and chronic heart failure. Eur Heart J 2008,29(10),1224-1240","journal-title":"Eur Heart J"},{"key":"ref=3","doi-asserted-by":"publisher","first-page":"191","DOI":"10.1016\/j.pharmthera.2010.04.005","volume":"128","author":"Bernardo B.C.","year":"2010","unstructured":"Bernardo B.C.; Weeks K.L.; Pretorius L.; McMullen J.R.; Molecular distinction between physiological and pathological cardiac hypertrophy: Experimental findings and therapeutic strategies. Pharmacol Ther 2010,128(1),191-227","journal-title":"Pharmacol Ther"},{"key":"ref=4","doi-asserted-by":"publisher","first-page":"1375","DOI":"10.1042\/CS20160170","volume":"131","author":"Dadson K.","year":"2017","unstructured":"Dadson K.; Hauck L.; Billia F.; Molecular mechanisms in cardiomyopathy. Clin Sci (Lond) 2017,131(13),1375-1392","journal-title":"Clin Sci (Lond)"},{"key":"ref=5","doi-asserted-by":"publisher","first-page":"983","DOI":"10.1007\/s00018-016-2373-0","volume":"74","author":"Haque Z.K.","year":"2017","unstructured":"Haque Z.K.; Wang D.Z.; How cardiomyocytes sense pathophysiological stresses for cardiac remodeling. Cell Mol Life Sci 2017,74(6),983-1000","journal-title":"Cell Mol Life Sci"},{"key":"ref=6","doi-asserted-by":"publisher","first-page":"1079","DOI":"10.1161\/01.RES.0000072977.86706.23","volume":"92","author":"Akazawa H.","year":"2003","unstructured":"Akazawa H.; Komuro I.; Roles of cardiac transcription factors in cardiac hypertrophy. Circ Res 2003,92(10),1079-1088","journal-title":"Circ Res"},{"key":"ref=7","doi-asserted-by":"publisher","first-page":"1505","DOI":"10.1007\/s10741-020-09959-3","volume":"26","author":"Lei H.","year":"2021","unstructured":"Lei H.; Hu J.; Sun K.; Xu D.; The role and molecular mechanism of epigenetics in cardiac hypertrophy. Heart Fail Rev 2021,26(6),1505-1514","journal-title":"Heart Fail Rev"},{"key":"ref=8","doi-asserted-by":"publisher","first-page":"241","DOI":"10.1016\/j.ejphar.2017.10.043","volume":"818","author":"Renu K.","year":"2018","unstructured":"Renu K.; v G A.; P B T.P.; Arunachalam S.; Molecular mechanism of doxorubicin-induced cardiomyopathy-An update. Eur J Pharmacol 2018,818,241-253","journal-title":"Eur J Pharmacol"},{"key":"ref=9","doi-asserted-by":"publisher","first-page":"132","DOI":"10.1002\/0470862637.ch9","volume":"259","author":"McKinsey T.A.","year":"2008","unstructured":"McKinsey T.A.; Olson E.N.; Dual roles of histone deacetylases in the control of cardiac growth. Novartis Found Symp 2008,259,132-145","journal-title":"Novartis Found Symp"},{"key":"ref=10","doi-asserted-by":"publisher","first-page":"20164","DOI":"10.1073\/pnas.1315155110","volume":"110","author":"Papait R.","year":"2013","unstructured":"Papait R.; Cattaneo P.; Kunderfranco P.; Greco C.; Carullo P.; Guffanti A.; Vigan&#xF2; V.; Stirparo G.G.; Latronico M.V.G.; Hasenfuss G.; Chen J.; Condorelli G.; Genome-wide analysis of histone marks identifying an epigenetic signature of promoters and enhancers underlying cardiac hypertrophy. Proc Natl Acad Sci USA 2013,110(50),20164-20169","journal-title":"Proc Natl Acad Sci USA"},{"key":"ref=11","doi-asserted-by":"publisher","first-page":"291","DOI":"10.1387\/ijdb.140077mb","volume":"58","author":"Kalish J.M.","year":"2014","unstructured":"Kalish J.M.; Jiang C.; Bartolomei M.S.; Epigenetics and imprinting in human disease. Int J Dev Biol 2014,58(2-3-4),291-298","journal-title":"Int J Dev Biol"},{"key":"ref=12","doi-asserted-by":"publisher","first-page":"3531","DOI":"10.1242\/dev.033902","volume":"136","author":"Schuettengruber B.","year":"2009","unstructured":"Schuettengruber B.; Cavalli G.; Recruitment of Polycomb group complexes and their role in the dynamic regulation of cell fate choice. Development 2009,136(21),3531-3542","journal-title":"Development"},{"key":"ref=13","doi-asserted-by":"publisher","first-page":"343","DOI":"10.1038\/ng.1068","volume":"44","author":"Delgado-Olgu&#xED;n P.","year":"2012","unstructured":"Delgado-Olgu&#xED;n P.; Huang Y.; Li X.; Christodoulou D.; Seidman C.E.; Seidman J.G.; Tarakhovsky A.; Bruneau B.G.; Epigenetic repression of cardiac progenitor gene expression by EZH2 is required for postnatal cardiac homeostasis. Nat Genet 2012,44(3),343-347","journal-title":"Nat Genet"},{"key":"ref=14","doi-asserted-by":"publisher","first-page":"2641","DOI":"10.1172\/JCI44641","volume":"121","author":"Stein A.B.","year":"2011","unstructured":"Stein A.B.; Jones T.A.; Herron T.J.; Patel S.R.; Day S.M.; Noujaim S.F.; Milstein M.L.; Klos M.; Furspan P.B.; Jalife J.; Dressler G.R.; Loss of H3K4 methylation destabilizes gene expression patterns and physiological functions in adult murine cardiomyocytes. J Clin Invest 2011,121(7),2641-2650","journal-title":"J Clin Invest"},{"key":"ref=15","doi-asserted-by":"publisher","first-page":"303","DOI":"10.1146\/annurev-pharmtox-010611-134712","volume":"52","author":"McKinsey T.A.","year":"2012","unstructured":"McKinsey T.A.; Therapeutic potential for HDAC inhibitors in the heart. Annu Rev Pharmacol Toxicol 2012,52(1),303-319","journal-title":"Annu Rev Pharmacol Toxicol"},{"key":"ref=16","doi-asserted-by":"publisher","first-page":"3","DOI":"10.1002\/0470029331.ch2","volume":"274","author":"Olson E.N.","year":"2008","unstructured":"Olson E.N.; Backs J.; McKinsey T.A.; Control of cardiac hypertrophy and heart failure by histone acetylation\/deacetylation. Novartis Found Symp 2008,274,3-19","journal-title":"Novartis Found Symp"},{"key":"ref=17","doi-asserted-by":"publisher","first-page":"600","DOI":"10.1002\/jcb.22185","volume":"107","author":"Marks P.A.","year":"2009","unstructured":"Marks P.A.; Xu W.S.; Histone deacetylase inhibitors: Potential in cancer therapy. J Cell Biochem 2009,107(4),600-608","journal-title":"J Cell Biochem"},{"key":"ref=18","doi-asserted-by":"publisher","first-page":"120","DOI":"10.1016\/j.yjmcc.2021.06.011","volume":"159","author":"Qin J.","year":"2021","unstructured":"Qin J.; Guo N.; Tong J.; Wang Z.; Function of histone methylation and acetylation modifiers in cardiac hypertrophy. J Mol Cell Cardiol 2021,159,120-129","journal-title":"J Mol Cell Cardiol"},{"key":"ref=19","doi-asserted-by":"publisher","first-page":"479","DOI":"10.1016\/S0092-8674(02)00861-9","volume":"110","author":"Zhang C.L.","year":"2002","unstructured":"Zhang C.L.; McKinsey T.A.; Chang S.; Antos C.L.; Hill J.A.; Olson E.N.; Class II histone deacetylases act as signal-responsive repressors of cardiac hypertrophy. Cell 2002,110(4),479-488","journal-title":"Cell"},{"key":"ref=20","doi-asserted-by":"publisher","first-page":"1790","DOI":"10.1101\/gad.1563807","volume":"21","author":"Montgomery R.L.","year":"2007","unstructured":"Montgomery R.L.; Davis C.A.; Potthoff M.J.; Haberland M.; Fielitz J.; Qi X.; Hill J.A.; Richardson J.A.; Olson E.N.; Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractility. Genes Dev 2007,21(14),1790-1802","journal-title":"Genes Dev"},{"key":"ref=21","doi-asserted-by":"publisher","first-page":"15","DOI":"10.1161\/01.RES.0000197782.21444.8f","volume":"98","author":"Backs J.","year":"2006","unstructured":"Backs J.; Olson E.N.; Control of cardiac growth by histone acetylation\/deacetylation. Circ Res 2006,98(1),15-24","journal-title":"Circ Res"},{"key":"ref=22","doi-asserted-by":"publisher","first-page":"7331","DOI":"10.1158\/1078-0432.CCR-18-4121","volume":"25","author":"Yap T.A.","year":"2019","unstructured":"Yap T.A.; Winter J.N.; Giulino-Roth L.; Longley J.; Lopez J.; Michot J.M.; Leonard J.P.; Ribrag V.; McCabe M.T.; Creasy C.L.; Stern M.; Pene Dumitrescu T.; Wang X.; Frey S.; Carver J.; Horner T.; Oh C.; Khaled A.; Dhar A.; Johnson P.W.M.; Phase I.; Phase I study of the novel enhancer of zeste homolog 2 (EZH2) inhibitor Gsk2816126 in patients with advanced hematologic and solid tumors. Clin Cancer Res 2019,25(24),7331-7339","journal-title":"Clin Cancer Res"},{"key":"ref=23","doi-asserted-by":"publisher","first-page":"128","DOI":"10.1038\/nm.4036","volume":"22","author":"Kim K.H.","year":"2016","unstructured":"Kim K.H.; Roberts C.W.M.; Targeting EZH2 in cancer. Nat Med 2016,22(2),128-134","journal-title":"Nat Med"},{"key":"ref=24","doi-asserted-by":"publisher","first-page":"e33453","DOI":"10.1371\/journal.pone.0033453","volume":"7","author":"Halsall J.","year":"2012","unstructured":"Halsall J.; Gupta V.; O\u2019Neill L.P.; Turner B.M.; Nightingale K.P.; Genes are often sheltered from the global histone hyperacetylation induced by HDAC inhibitors. PLoS One 2012,7(3),e33453","journal-title":"PLoS One"},{"key":"ref=25","doi-asserted-by":"publisher","first-page":"708","DOI":"10.1101\/gr.5540007","volume":"17","author":"Rada-Iglesias A.","year":"2007","unstructured":"Rada-Iglesias A.; Enroth S.; Ameur A.; Koch C.M.; Clelland G.K.; Respuela-Alonso P.; Wilcox S.; Dovey O.M.; Ellis P.D.; Langford C.F.; Dunham I.; Komorowski J.; Wadelius C.; Butyrate mediates decrease of histone acetylation centered on transcription start sites and down-regulation of associated genes. Genome Res 2007,17(6),708-719","journal-title":"Genome Res"},{"key":"ref=26","doi-asserted-by":"publisher","first-page":"1271","DOI":"10.1101\/gr.168781.113","volume":"24","author":"Rafehi H.","year":"2014","unstructured":"Rafehi H.; Balcerczyk A.; Lunke S.; Kaspi A.; Ziemann M.; Kn H.; Okabe J.; Khurana I.; Ooi J.; Khan A.W.; Du X.J.; Chang L.; Haviv I.; Keating S.T.; Karagiannis T.C.; El-Osta A.; Vascular histone deacetylation by pharmacological HDAC inhibition. Genome Res 2014,24(8),1271-1284","journal-title":"Genome Res"},{"key":"ref=27","doi-asserted-by":"publisher","first-page":"28930","DOI":"10.1074\/jbc.M303113200","volume":"278","author":"Antos C.L.","year":"2003","unstructured":"Antos C.L.; McKinsey T.A.; Dreitz M.; Hollingsworth L.M.; Zhang C.L.; Schreiber K.; Rindt H.; Gorczynski R.J.; Olson E.N.; Dose-dependent blockade to cardiomyocyte hypertrophy by histone deacetylase inhibitors. J Biol Chem 2003,278(31),28930-28937","journal-title":"J Biol Chem"},{"key":"ref=28","doi-asserted-by":"publisher","first-page":"4123","DOI":"10.1073\/pnas.1015081108","volume":"108","author":"Cao D.J.","year":"2011","unstructured":"Cao D.J.; Wang Z.V.; Battiprolu P.K.; Jiang N.; Morales C.R.; Kong Y.; Rothermel B.A.; Gillette T.G.; Hill J.A.; Histone deacetylase (HDAC) inhibitors attenuate cardiac hypertrophy by suppressing autophagy. Proc Natl Acad Sci USA 2011,108(10),4123-4128","journal-title":"Proc Natl Acad Sci USA"},{"key":"ref=29","doi-asserted-by":"publisher","first-page":"108","DOI":"10.1038\/s41556-019-0446-7","volume":"22","author":"Wang L.","year":"2020","unstructured":"Wang L.; Yu P.; Zhou B.; Song J.; Li Z.; Zhang M.; Guo G.; Wang Y.; Chen X.; Han L.; Hu S.; Single-cell reconstruction of the adult human heart during heart failure and recovery reveals the cellular landscape underlying cardiac function. Nat Cell Biol 2020,22(1),108-119","journal-title":"Nat Cell Biol"},{"key":"ref=30","doi-asserted-by":"publisher","first-page":"209","DOI":"10.2217\/epi.14.11","volume":"6","author":"Meier B.C.","year":"2014","unstructured":"Meier B.C.; Wagner B.K.; Inhibition of HDAC3 as a strategy for developing novel diabetes therapeutics. Epigenomics 2014,6(2),209-214","journal-title":"Epigenomics"},{"key":"ref=31","doi-asserted-by":"publisher","first-page":"34","DOI":"10.1016\/j.pharmthera.2013.05.010","volume":"140","author":"Harrison I.F.","year":"2013","unstructured":"Harrison I.F.; Dexter D.T.; Epigenetic targeting of histone deacetylase: Therapeutic potential in Parkinson\u2019s disease? Pharmacol Ther 2013,140(1),34-52","journal-title":"Pharmacol Ther"},{"key":"ref=32","doi-asserted-by":"publisher","first-page":"1235","DOI":"10.3390\/ph15101235","volume":"15","author":"Bouyahya A.","year":"2022","unstructured":"Bouyahya A.; El Omari N.; Bakha M.; Aanniz T.; El Menyiy N.; El Hachlafi N.; El Baaboua A.; El-Shazly M.; Alshahrani M.M.; Al Awadh A.A.; Lee L.H.; Benali T.; Mubarak M.S.; Pharmacological properties of trichostatin A, focusing on the anticancer potential: A comprehensive review. Pharmaceuticals 2022,15(10),1235","journal-title":"Pharmaceuticals"},{"key":"ref=33","doi-asserted-by":"publisher","first-page":"455","DOI":"10.1161\/CIRCULATIONAHA.112.103176","volume":"126","author":"Zhao L.","year":"2012","unstructured":"Zhao L.; Chen C.N.; Hajji N.; Oliver E.; Cotroneo E.; Wharton J.; Wang D.; Li M.; McKinsey T.A.; Stenmark K.R.; Wilkins M.R.; Histone deacetylation inhibition in pulmonary hypertension: Therapeutic potential of valproic acid and suberoylanilide hydroxamic acid. Circulation 2012,126(4),455-467","journal-title":"Circulation"},{"key":"ref=34","doi-asserted-by":"publisher","first-page":"226","DOI":"10.1111\/1440-1681.13022","volume":"46","author":"Lee E.","year":"2019","unstructured":"Lee E.; Lee H.A.; Kim M.; Do G.; Cho H.M.; Kim G.J.; Jung H.; Song J.H.; Cho J.M.; Kim I.; Upregulation of C\/EBP&#x3B2; and TSC2 by an HDAC inhibitor CG200745 protects heart from DOCA-induced hypertrophy. Clin Exp Pharmacol Physiol 2019,46(3),226-236","journal-title":"Clin Exp Pharmacol Physiol"},{"key":"ref=35","doi-asserted-by":"publisher","first-page":"863","DOI":"10.1172\/JCI19137","volume":"112","author":"Kook H.","year":"2003","unstructured":"Kook H.; Lepore J.J.; Gitler A.D.; Lu M.M.; Wing-Man Yung W.; Mackay J.; Zhou R.; Ferrari V.; Gruber P.; Epstein J.A.; Cardiac hypertrophy and histone deacetylase\u2013dependent transcriptional repression mediated by the atypical homeodomain protein Hop. J Clin Invest 2003,112(6),863-871","journal-title":"J Clin Invest"},{"key":"ref=36","doi-asserted-by":"publisher","first-page":"760","DOI":"10.1253\/circj.CJ-09-0580","volume":"74","author":"Cho Y.K.","year":"2010","unstructured":"Cho Y.K.; Eom G.H.; Kee H.J.; Kim H.S.; Choi W.Y.; Nam K.I.; Ma J.S.; Kook H.; Sodium valproate, a histone deacetylase inhibitor, but not captopril, prevents right ventricular hypertrophy in rats. Circ J 2010,74(4),760-770","journal-title":"Circ J"},{"key":"ref=37","doi-asserted-by":"publisher","first-page":"343","DOI":"10.1038\/nature09784","volume":"469","author":"Margueron R.","year":"2011","unstructured":"Margueron R.; Reinberg D.; The Polycomb complex PRC2 and its mark in life. Nature 2011,469(7330),343-349","journal-title":"Nature"},{"key":"ref=38","doi-asserted-by":"publisher","first-page":"406","DOI":"10.1161\/CIRCRESAHA.111.252205","volume":"110","author":"He A.","year":"2012","unstructured":"He A.; Ma Q.; Cao J.; von Gise A.; Zhou P.; Xie H.; Zhang B.; Hsing M.; Christodoulou D.C.; Cahan P.; Daley G.Q.; Kong S.W.; Orkin S.H.; Seidman C.E.; Seidman J.G.; Pu W.T.; Polycomb repressive complex 2 regulates normal development of the mouse heart. Circ Res 2012,110(3),406-415","journal-title":"Circ Res"},{"key":"ref=39","doi-asserted-by":"publisher","first-page":"372","DOI":"10.1161\/CIRCRESAHA.111.263145","volume":"110","author":"Dobreva G.","year":"2012","unstructured":"Dobreva G.; Braun T.; When silence is broken: Polycomb group proteins in heart development. Circ Res 2012,110(3),372-374","journal-title":"Circ Res"},{"key":"ref=40","doi-asserted-by":"publisher","first-page":"1131","DOI":"10.1038\/nm.4179","volume":"22","author":"Wang Z.","year":"2016","unstructured":"Wang Z.; Zhang X.J.; Ji Y.X.; Zhang P.; Deng K.Q.; Gong J.; Ren S.; Wang X.; Chen I.; Wang H.; Gao C.; Yokota T.; Ang Y.S.; Li S.; Cass A.; Vondriska T.M.; Li G.; Deb A.; Srivastava D.; Yang H.T.; Xiao X.; Li H.; Wang Y.; The long noncoding RNA Chaer defines an epigenetic checkpoint in cardiac hypertrophy. Nat Med 2016,22(10),1131-1139","journal-title":"Nat Med"},{"key":"ref=41","doi-asserted-by":"publisher","first-page":"585691","DOI":"10.3389\/fcvm.2021.585691","volume":"8","author":"Wang S.","year":"2021","unstructured":"Wang S.; Guo N.; Li S.; He Y.; Zheng D.; Li L.; Wang Z.; EZH2 dynamically associates with non-coding rnas in mouse hearts after acute Angiotensin II treatment. Front Cardiovasc Med 2021,8,585691","journal-title":"Front Cardiovasc Med"},{"key":"ref=42","doi-asserted-by":"publisher","first-page":"286","DOI":"10.1016\/S0955-0674(02)00335-6","volume":"14","author":"Lachner M.","year":"2002","unstructured":"Lachner M.; Jenuwein T.; The many faces of histone lysine methylation. Curr Opin Cell Biol 2002,14(3),286-298","journal-title":"Curr Opin Cell Biol"},{"key":"ref=43","doi-asserted-by":"publisher","first-page":"5288","DOI":"10.1038\/ncomms6288","volume":"5","author":"Gilsbach R.","year":"2014","unstructured":"Gilsbach R.; Preissl S.; Gr&#xFC;ning B.A.; Schnick T.; Burger L.; Benes V.; W&#xFC;rch A.; B&#xF6;nisch U.; G&#xFC;nther S.; Backofen R.; Fleischmann B.K.; Sch&#xFC;beler D.; Hein L.; Dynamic DNA methylation orchestrates cardiomyocyte development, maturation and disease. Nat Commun 2014,5(1),5288","journal-title":"Nat Commun"},{"key":"ref=44","doi-asserted-by":"publisher","first-page":"62","DOI":"10.1038\/nature09130","volume":"466","author":"Hang C.T.","year":"2010","unstructured":"Hang C.T.; Yang J.; Han P.; Cheng H.L.; Shang C.; Ashley E.; Zhou B.; Chang C.P.; Chromatin regulation by Brg1 underlies heart muscle development and disease. Nature 2010,466(7302),62-67","journal-title":"Nature"},{"key":"ref=45","doi-asserted-by":"publisher","first-page":"102","DOI":"10.1038\/nature13596","volume":"514","author":"Han P.","year":"2014","unstructured":"Han P.; Li W.; Lin C.H.; Yang J.; Shang C.; Nurnberg S.T.; Jin K.K.; Xu W.; Lin C.Y.; Lin C.J.; Xiong Y.; Chien H.C.; Zhou B.; Ashley E.; Bernstein D.; Chen P.S.; Chen H.S.V.; Quertermous T.; Chang C.P.; A long noncoding RNA protects the heart from pathological hypertrophy. Nature 2014,514(7520),102-106","journal-title":"Nature"}],"container-title":["Current Drug Targets"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.eurekaselect.com\/article\/download?doi=10.2174\/1389450124666230124094936","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.eurekaselect.com\/213072\/article","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/www.eurekaselect.com\/article\/download?doi=10.2174\/1389450124666230124094936","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,6,13]],"date-time":"2023-06-13T08:35:30Z","timestamp":1686645330000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.eurekaselect.com\/213072\/article"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2023,3]]},"references-count":45,"journal-issue":{"issue":"4","published-print":{"date-parts":[[2023,3]]}},"alternative-id":["LiveAll1"],"URL":"https:\/\/doi.org\/10.2174\/1389450124666230124094936","relation":{},"ISSN":["1389-4501"],"issn-type":[{"value":"1389-4501","type":"print"}],"subject":[],"published":{"date-parts":[[2023,3]]},"assertion":[{"value":"Peer Reviewed","order":0,"name":"review_status","label":"Review Status","group":{"name":"peer_review_details","label":"Peer Review Details"}},{"value":"Single blind","order":1,"name":"review_process","label":"Review Process","group":{"name":"peer_review_details","label":"Peer Review Details"}},{"value":"Checked with iThenticate","order":0,"name":"screening_status","label":"Screening Status","group":{"name":"plagiarism_screening","label":"Plagiarism Screening"}},{"value":"2022-10-15","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-01-02","order":1,"name":"revised","label":"Revised","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-01-02","order":2,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2023-03-30","order":3,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}