{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,24]],"date-time":"2026-10-24T00:54:00Z","timestamp":1792803240623,"version":"4.5.0"},"reference-count":58,"publisher":"IMR Press","issue":"5","license":[{"start":{"date-parts":[[2026,5,28]],"date-time":"2026-05-28T00:00:00Z","timestamp":1779926400000},"content-version":"unspecified","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"Affiliated Hospital of Nantong University Research Physician Development Fund","award":["YJXYY202204-YSB59"],"award-info":[{"award-number":["YJXYY202204-YSB59"]}],"id":[{"id":"https:\/\/ror.org\/001rahr89","id-type":"ROR","asserted-by":"crossref"}]},{"name":"Postgraduate Research & Practice Innovation Program of Jiangsu Province in 2023","award":["SJCX23_1791"],"award-info":[{"award-number":["SJCX23_1791"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Pharmazie"],"abstract":"<jats:p>Objective:Histone deacetylase 1 (HDAC1) exacerbates ventricular remodeling and heart failure by promoting myocardial peroxidative damage. Thus, this study aimed to investigate whether the HDAC1 inhibitor mocetinostat alleviates pathological cardiac hypertrophy via suppressing ferroptosis and to elucidate the potential mechanisms involving the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway.Methods:Primary cardiomyocytes were stimulated with phenylephrine (PE) to induce hypertrophy and ferroptosis in vitro, with or without mocetinostat treatment. The Nrf2 inhibitor ML385 was used to verify pathway specificity. In vivo, a mouse model of pressure-overload-induced cardiac hypertrophy was established using a transverse aortic constriction (TAC)-induced approach. Mocetinostat was administered to evaluate its therapeutic effects. Ferroptosis markers including lipid peroxidation, iron accumulation, and levels of ferroptosis-related proteins, were assessed. The acetylation and nuclear translocation of Nrf2, as well as the expression of the associated downstream targets (Solute carrier family 7 member 11 (SLC7A11), glutathione peroxidase 4 (GPX4), ferroportin, ferritin heavy chain 1 (FTH1), heme oxygenase-1 (HO-1)), were analyzed.Results:Mocetinostat treatment significantly ameliorated PE-induced cardiomyocyte hypertrophy and ferroptosis in vitro and attenuated TAC-induced cardiac hypertrophy and fibrosis in vivo. Mechanistically, mocetinostat facilitated Nrf2 acetylation and promoted Nrf2 nuclear translocation, leading to the transcriptional activation of downstream antioxidant targets and subsequent inhibition of lipid peroxidation. The protective effects of mocetinostat were abrogated by the Nrf2 inhibitor ML385.Conclusion:This study demonstrates that mocetinostat attenuates pathological cardiac hypertrophy by inhibiting ferroptosis through activation of the Nrf2 pathway . These findings indicate the potential of mocetinostat as a therapeutic strategy for delaying heart failure progression.<\/jats:p>","DOI":"10.31083\/pharmazie51659","type":"journal-article","created":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T08:35:36Z","timestamp":1780130136000},"source":"Crossref","is-referenced-by-count":2,"title":["Mocetinostat Ameliorates Pathological Cardiac Hypertrophy via Suppression of Ferroptosis Through Nrf2 Pathway"],"prefix":"10.31083","volume":"81","author":[{"ORCID":"https:\/\/orcid.org\/0009-0006-9654-5639","authenticated-orcid":true,"given":"Jingyu","family":"Li","sequence":"first","affiliation":[{"name":"Medical School, Nantong University, 226000 Nantong, Jiangsu, China"},{"name":"Department of Cardiology, Affiliated Hospital of Nantong University, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-4952-9917","authenticated-orcid":true,"given":"Hanrui","family":"Sun","sequence":"additional","affiliation":[{"name":"Medical School, Nantong University, 226000 Nantong, Jiangsu, China"},{"name":"Department of Cardiology, Affiliated Hospital of Nantong University, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-0927-8109","authenticated-orcid":true,"given":"Jiabin","family":"Zhou","sequence":"additional","affiliation":[{"name":"Department of Cardiovascular Medicine, Affiliated Wuxi People\u2019s Hospital of Nanjing Medical University, Wuxi People\u2019s Hospital, 214023 Wuxi, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3627-8314","authenticated-orcid":true,"given":"Jiayu","family":"Shi","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Affiliated Hospital of Nantong University, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-4819-6610","authenticated-orcid":true,"given":"Peng","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Nantong Sixth People\u2019s Hospital, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-7893-5143","authenticated-orcid":true,"given":"Chen","family":"Wang","sequence":"additional","affiliation":[{"name":"Medical School, Nantong University, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0002-0951-3964","authenticated-orcid":true,"given":"Chuchu","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Jiangyin Hospital of Traditional Chinese Medicine, 214400 Wuxi, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-9126-0323","authenticated-orcid":true,"given":"Pengyang","family":"Gu","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Affiliated Hospital of Nantong University, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0001-3321-1811","authenticated-orcid":true,"given":"Xinglin","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Cardiology, Fujian Medical University Union Hospital, 350001 Fuzhou, Fujian, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-3471-3592","authenticated-orcid":true,"given":"Qing","family":"Gong","sequence":"additional","affiliation":[{"name":"Medical School, Nantong University, 226000 Nantong, Jiangsu, China"},{"name":"Department of Cardiology, Affiliated Hospital of Nantong University, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0003-0327-4541","authenticated-orcid":true,"given":"Anzhen","family":"Xu","sequence":"additional","affiliation":[{"name":"Medical School, Nantong University, 226000 Nantong, Jiangsu, China"},{"name":"Department of Cardiology, Affiliated Hospital of Nantong University, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0007-5802-6288","authenticated-orcid":true,"given":"Yanbo","family":"Li","sequence":"additional","affiliation":[{"name":"Medical School, Nantong University, 226000 Nantong, Jiangsu, China"},{"name":"Department of Cardiology, Affiliated Hospital of Nantong University, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2849-6488","authenticated-orcid":true,"given":"Qi","family":"Lu","sequence":"additional","affiliation":[{"name":"Medical School, Nantong University, 226000 Nantong, Jiangsu, China"},{"name":"Department of Cardiology, Affiliated Hospital of Nantong University, 226000 Nantong, Jiangsu, China"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"16242","published-online":{"date-parts":[[2026,5,28]]},"reference":[{"key":"ref1","doi-asserted-by":"publisher","unstructured":"Nakamura M, Sadoshima J. Mechanisms of physiological and pathological cardiac hypertrophy. Nature Reviews. Cardiology, 2018, 15: pp. 387-407.","DOI":"10.1038\/s41569-018-0007-y"},{"key":"ref2","doi-asserted-by":"publisher","unstructured":"Tham YK, Bernardo BC, Ooi JYY, Weeks KL, McMullen JR. Pathophysiology of cardiac hypertrophy and heart failure: signaling pathways and novel therapeutic targets. Archives of Toxicology, 2015, 89: pp. 1401-1438.","DOI":"10.1007\/s00204-015-1477-x"},{"key":"ref3","doi-asserted-by":"publisher","unstructured":"Luo Q, Zhang Q, Kong Y, Wang S, Wei Q. Heart failure, inflammation and exercise. International Journal of Biological Sciences, 2025, 21: pp. 3324-3350.","DOI":"10.7150\/ijbs.109917"},{"key":"ref4","doi-asserted-by":"publisher","unstructured":"Dixon SJ, Lemberg KM, Lamprecht MR, Skouta R, Zaitsev EM, Gleason CE, et al. Ferroptosis: an iron-dependent form of nonapoptotic cell death. Cell, 2012, 149: pp. 1060-1072.","DOI":"10.1016\/j.cell.2012.03.042"},{"key":"ref5","doi-asserted-by":"publisher","unstructured":"Mou Y, Wang J, Wu J, He D, Zhang C, Duan C, et al. Ferroptosis, a new form of cell death: opportunities and challenges in cancer. Journal of Hematology & Oncology, 2019, 12: pp. 34.","DOI":"10.1186\/s13045-019-0720-y"},{"key":"ref6","doi-asserted-by":"publisher","unstructured":"Gao M, Monian P, Pan Q, Zhang W, Xiang J, Jiang X. Ferroptosis is an autophagic cell death process. Cell Research, 2016, 26: pp. 1021-1032.","DOI":"10.1038\/cr.2016.95"},{"key":"ref7","doi-asserted-by":"publisher","unstructured":"Ingold I, Berndt C, Schmitt S, Doll S, Poschmann G, Buday K, et al. Selenium Utilization by GPX4 Is Required to Prevent Hydroperoxide-Induced Ferroptosis. Cell, 2018, 172: pp. 409-422.e21.","DOI":"10.1016\/j.cell.2017.11.048"},{"key":"ref8","doi-asserted-by":"publisher","unstructured":"Chang LC, Chiang SK, Chen SE, Yu YL, Chou RH, Chang WC. Heme oxygenase-1 mediates BAY 11-7085 induced ferroptosis. Cancer Letters, 2018, 416: pp. 124-137.","DOI":"10.1016\/j.canlet.2017.12.025"},{"key":"ref9","doi-asserted-by":"publisher","unstructured":"Cui J, Chen Y, Yang Q, Zhao P, Yang M, Wang X, et al. Protosappanin A Protects DOX-Induced Myocardial Injury and Cardiac Dysfunction by Targeting ACSL4\/FTH1 Axis-Dependent Ferroptosis. Advanced Science (Weinheim, Baden-Wurttemberg, Germany), 2024, 11: pp. e2310227.","DOI":"10.1002\/advs.202310227"},{"key":"ref10","doi-asserted-by":"publisher","unstructured":"Liu B, Zhao C, Li H, Chen X, Ding Y, Xu S. Puerarin protects against heart failure induced by pressure overload through mitigation of ferroptosis. Biochemical and Biophysical Research Communications, 2018, 497: pp. 233-240.","DOI":"10.1016\/j.bbrc.2018.02.061"},{"key":"ref11","doi-asserted-by":"publisher","unstructured":"Zhang X, Zheng C, Gao Z, Chen H, Li K, Wang L, et al. SLC7A11\/xCT Prevents Cardiac Hypertrophy by Inhibiting Ferroptosis. Cardiovascular Drugs and Therapy, 2022, 36: pp. 437-447.","DOI":"10.1007\/s10557-021-07220-z"},{"key":"ref12","doi-asserted-by":"publisher","unstructured":"Ito J, Omiya S, Rusu MC, Ueda H, Murakawa T, Tanada Y, et al. Iron derived from autophagy-mediated ferritin degradation induces cardiomyocyte death and heart failure in mice. elife, 2021, 10: pp. e62174.","DOI":"10.7554\/eLife.62174"},{"key":"ref13","doi-asserted-by":"publisher","unstructured":"Narita T, Weinert BT, Choudhary C. Functions and mechanisms of non-histone protein acetylation. Nature Reviews. Molecular Cell Biology, 2019, 20: pp. 156-174.","DOI":"10.1038\/s41580-018-0081-3"},{"key":"ref14","doi-asserted-by":"publisher","unstructured":"Li Y, Seto E. HDACs and HDAC Inhibitors in Cancer Development and Therapy. Cold Spring Harbor Perspectives in Medicine, 2016, 6: pp. a026831.","DOI":"10.1101\/cshperspect.a026831"},{"key":"ref15","doi-asserted-by":"publisher","unstructured":"Zhou J, Shi J, Xu P, Wu G, Wang C, Li J, et al. Establishment of Ferroptosis-Associated Molecular Subtypes and Hub Genes Related to the Immune Microenvironment of Heart Failure. Frontiers in Bioscience (Landmark Edition), 2023, 28: pp. 246.","DOI":"10.31083\/j.fbl2810246"},{"key":"ref16","doi-asserted-by":"publisher","unstructured":"Montgomery RL, Davis CA, Potthoff MJ, Haberland M, Fielitz J, Qi X, et al. Histone deacetylases 1 and 2 redundantly regulate cardiac morphogenesis, growth, and contractility. Genes & Development, 2007, 21: pp. 1790-1802.","DOI":"10.1101\/gad.1563807"},{"key":"ref17","doi-asserted-by":"publisher","unstructured":"Gallo P, Latronico MVG, Gallo P, Grimaldi S, Borgia F, Todaro M, et al. Inhibition of class I histone deacetylase with an apicidin derivative prevents cardiac hypertrophy and failure. Cardiovascular Research, 2008, 80: pp. 416-424.","DOI":"10.1093\/cvr\/cvn215"},{"key":"ref18","doi-asserted-by":"publisher","unstructured":"Fournel M, Bonfils C, Hou Y, Yan PT, Trachy-Bourget MC, Kalita A, et al. MGCD0103, a novel isotype-selective histone deacetylase inhibitor, has broad spectrum antitumor activity in vitro and in vivo. Molecular Cancer Therapeutics, 2008, 7: pp. 759-768.","DOI":"10.1158\/1535-7163.MCT-07-2026"},{"key":"ref19","doi-asserted-by":"publisher","unstructured":"Nural-Guvener H, Zakharova L, Feehery L, Sljukic S, Gaballa M. Anti-Fibrotic Effects of Class I HDAC Inhibitor, Mocetinostat Is Associated with IL-6\/Stat3 Signaling in Ischemic Heart Failure. International Journal of Molecular Sciences, 2015, 16: pp. 11482-11499.","DOI":"10.3390\/ijms160511482"},{"key":"ref20","doi-asserted-by":"publisher","unstructured":"Kim GJ, Jung H, Lee E, Chung SW. Histone deacetylase inhibitor, mocetinostat, regulates cardiac remodelling and renin-angiotensin system activity in rats with transverse aortic constriction-induced pressure overload cardiac hypertrophy. Reviews in Cardiovascular Medicine, 2021, 22: pp. 1037-1045.","DOI":"10.31083\/j.rcm2203113"},{"key":"ref21","doi-asserted-by":"publisher","unstructured":"Zhou M, Sun X, Wang C, Wang F, Fang C, Hu Z. PFKM inhibits doxorubicin-induced cardiotoxicity by enhancing oxidative phosphorylation and glycolysis. Scientific Reports, 2022, 12: pp. 11684.","DOI":"10.1038\/s41598-022-15743-0"},{"key":"ref22","doi-asserted-by":"publisher","unstructured":"Bellezza I, Giambanco I, Minelli A, Donato R. Nrf2-Keap1 signaling in oxidative and reductive stress. Biochimica et Biophysica Acta. Molecular Cell Research, 2018, 1865: pp. 721-733.","DOI":"10.1016\/j.bbamcr.2018.02.010"},{"key":"ref23","doi-asserted-by":"publisher","unstructured":"Yamamoto M, Kensler TW, Motohashi H. The KEAP1-NRF2 System: a Thiol-Based Sensor-Effector Apparatus for Maintaining Redox Homeostasis. Physiological Reviews, 2018, 98: pp. 1169-1203.","DOI":"10.1152\/physrev.00023.2017"},{"key":"ref24","doi-asserted-by":"publisher","unstructured":"Imam MU, Zhang S, Ma J, Wang H, Wang F. Antioxidants Mediate Both Iron Homeostasis and Oxidative Stress. Nutrients, 2017, 9: pp. 671.","DOI":"10.3390\/nu9070671"},{"key":"ref25","doi-asserted-by":"publisher","unstructured":"Fan Z, Wirth AK, Chen D, Wruck CJ, Rauh M, Buchfelder M, et al. Nrf2-Keap1 pathway promotes cell proliferation and diminishes ferroptosis. Oncogenesis, 2017, 6: pp. e371.","DOI":"10.1038\/oncsis.2017.65"},{"key":"ref26","doi-asserted-by":"publisher","unstructured":"Loboda A, Damulewicz M, Pyza E, Jozkowicz A, Dulak J. Role of Nrf2\/HO-1 system in development, oxidative stress response and diseases: an evolutionarily conserved mechanism. Cellular and Molecular Life Sciences : CMLS, 2016, 73: pp. 3221-3247.","DOI":"10.1007\/s00018-016-2223-0"},{"key":"ref27","doi-asserted-by":"publisher","unstructured":"Wang X, Chen X, Zhou W, Men H, Bao T, Sun Y, et al. Ferroptosis is essential for diabetic cardiomyopathy and is prevented by sulforaphane via AMPK\/NRF2 pathways. Acta Pharmaceutica Sinica. B, 2022, 12: pp. 708-722.","DOI":"10.1016\/j.apsb.2021.10.005"},{"key":"ref28","doi-asserted-by":"publisher","unstructured":"Ma S, Henson ES, Chen Y, Gibson SB. Ferroptosis is induced following siramesine and lapatinib treatment of breast cancer cells. Cell Death & Disease, 2016, 7: pp. e2307.","DOI":"10.1038\/cddis.2016.208"},{"key":"ref29","doi-asserted-by":"publisher","unstructured":"Jiang Z, Yang H, Ni W, Gao X, Pei X, Jiang H, et al. Attenuation of neuronal ferroptosis in intracerebral hemorrhage by inhibiting HDAC1\/2: Microglial heterogenization via the Nrf2\/HO1 pathway. CNS Neuroscience & Therapeutics, 2024, 30: pp. e14646.","DOI":"10.1111\/cns.14646"},{"key":"ref30","doi-asserted-by":"publisher","unstructured":"Zhou J, Yu T, Wu G, Xu P, Wang C, Su Y, et al. Pyrroloquinoline quinone modulates YAP-related anti-ferroptotic activity to protect against myocardial hypertrophy. Frontiers in Pharmacology, 2022, 13: pp. 977385.","DOI":"10.3389\/fphar.2022.977385"},{"key":"ref31","doi-asserted-by":"publisher","unstructured":"Smiley ST, Reers M, Mottola-Hartshorn C, Lin M, Chen A, Smith TW, et al. Intracellular heterogeneity in mitochondrial membrane potentials revealed by a J-aggregate-forming lipophilic cation JC-1. Proceedings of the National Academy of Sciences of the United States of America, 1991, 88: pp. 3671-3675.","DOI":"10.1073\/pnas.88.9.3671"},{"key":"ref32","doi-asserted-by":"publisher","unstructured":"Stockwell BR, Friedmann Angeli JP, Bayir H, Bush AI, Conrad M, Dixon SJ, et al. Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease. Cell, 2017, 171: pp. 273-285.","DOI":"10.1016\/j.cell.2017.09.021"},{"key":"ref33","doi-asserted-by":"publisher","unstructured":"Yang WS, Stockwell BR. Ferroptosis: Death by Lipid Peroxidation. Trends in Cell Biology, 2016, 26: pp. 165-176.","DOI":"10.1016\/j.tcb.2015.10.014"},{"key":"ref34","doi-asserted-by":"publisher","unstructured":"Cheng X, Zhang J, Xiao Y, Wang Z, He J, Ke M, et al. Mitochondrial Regulation of Ferroptosis in Cancer Therapy. International Journal of Molecular Sciences, 2023, 24: pp. 10037.","DOI":"10.3390\/ijms241210037"},{"key":"ref35","doi-asserted-by":"publisher","unstructured":"Ru Q, Li Y, Chen L, Wu Y, Min J, Wang F. Iron homeostasis and ferroptosis in human diseases: mechanisms and therapeutic prospects. Signal Transduction and Targeted Therapy, 2024, 9: pp. 271.","DOI":"10.1038\/s41392-024-01969-z"},{"key":"ref36","doi-asserted-by":"publisher","unstructured":"Kagan VE, Mao G, Qu F, Angeli JPF, Doll S, Croix CS, et al. Oxidized arachidonic and adrenic PEs navigate cells to ferroptosis. Nature Chemical Biology, 2017, 13: pp. 81-90.","DOI":"10.1038\/nchembio.2238"},{"key":"ref37","doi-asserted-by":"publisher","unstructured":"Zhang Y, Xin L, Xiang M, Shang C, Wang Y, Wang Y, et al. The molecular mechanisms of ferroptosis and its role in cardiovascular disease. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, 2022, 145: pp. 112423.","DOI":"10.1016\/j.biopha.2021.112423"},{"key":"ref38","doi-asserted-by":"publisher","unstructured":"Zhang K, Tian XM, Li W, Hao LY. Ferroptosis in cardiac hypertrophy and heart failure. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, 2023, 168: pp. 115765.","DOI":"10.1016\/j.biopha.2023.115765"},{"key":"ref39","doi-asserted-by":"publisher","unstructured":"Zhou H, Ren J, Toan S, Mui D. Role of mitochondrial quality surveillance in myocardial infarction: From bench to bedside. Ageing Research Reviews, 2021, 66: pp. 101250.","DOI":"10.1016\/j.arr.2020.101250"},{"key":"ref40","doi-asserted-by":"publisher","unstructured":"Mao C, Liu X, Zhang Y, Lei G, Yan Y, Lee H, et al. DHODH-mediated ferroptosis defence is a targetable vulnerability in cancer. Nature, 2021, 593: pp. 586-590.","DOI":"10.1038\/s41586-021-03539-7"},{"key":"ref41","doi-asserted-by":"publisher","unstructured":"Wang P, Cui Y, Ren Q, Yan B, Zhao Y, Yu P, et al. Mitochondrial ferritin attenuates cerebral ischaemia\/reperfusion injury by inhibiting ferroptosis. Cell Death & Disease, 2021, 12: pp. 447.","DOI":"10.1038\/s41419-021-03725-5"},{"key":"ref42","doi-asserted-by":"publisher","unstructured":"Shin D, Lee J, You JH, Kim D, Roh JL. Dihydrolipoamide dehydrogenase regulates cystine deprivation-induced ferroptosis in head and neck cancer. Redox Biology, 2020, 30: pp. 101418.","DOI":"10.1016\/j.redox.2019.101418"},{"key":"ref43","doi-asserted-by":"publisher","unstructured":"Chen QM. Nrf2 for cardiac protection: pharmacological options against oxidative stress. Trends in Pharmacological Sciences, 2021, 42: pp. 729-744.","DOI":"10.1016\/j.tips.2021.06.005"},{"key":"ref44","doi-asserted-by":"publisher","unstructured":"Fang X, Wang H, Han D, Xie E, Yang X, Wei J, et al. Ferroptosis as a target for protection against cardiomyopathy. Proceedings of the National Academy of Sciences of the United States of America, 2019, 116: pp. 2672-2680.","DOI":"10.1073\/pnas.1821022116"},{"key":"ref45","doi-asserted-by":"publisher","unstructured":"Jiang X, Stockwell BR, Conrad M. Ferroptosis: mechanisms, biology and role in disease. Nature Reviews. Molecular Cell Biology, 2021, 22: pp. 266-282.","DOI":"10.1038\/s41580-020-00324-8"},{"key":"ref46","doi-asserted-by":"publisher","unstructured":"Li B, Zhang Y, Fu Y, Zheng Y, Dou K, Sun W. Modulation of Ferroptosis by the Irx3-Etfa Pathway Protects Against Cardiac Hypertrophy. FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology, 2026, 40: pp. e71524.","DOI":"10.1096\/fj.202502033RR"},{"key":"ref47","doi-asserted-by":"publisher","unstructured":"Zheng R, Song W, Wang C, Du X, Liu C, Sun X, et al. Deubiquitinase OTUD7B stabilizes HNF4\u03b1 to alleviate pressure overload-induced cardiac hypertrophy by regulating fatty acid oxidation and inhibiting ferroptosis. Biomarker Research, 2025, 13: pp. 53.","DOI":"10.1186\/s40364-025-00766-2"},{"key":"ref48","doi-asserted-by":"publisher","unstructured":"Li P, Ge J, Li H. Lysine acetyltransferases and lysine deacetylases as targets for cardiovascular disease. Nature Reviews. Cardiology, 2020, 17: pp. 96-115.","DOI":"10.1038\/s41569-019-0235-9"},{"key":"ref49","doi-asserted-by":"publisher","unstructured":"Liu YQ, Yang Q, He GW. Post-translational acylation of proteins in cardiac hypertrophy. Nature Reviews. Cardiology, 2025, 22: pp. 944-960.","DOI":"10.1038\/s41569-025-01150-1"},{"key":"ref50","doi-asserted-by":"publisher","unstructured":"Cao DJ, Wang ZV, Battiprolu PK, Jiang N, Morales CR, Kong Y, et al. Histone deacetylase (HDAC) inhibitors attenuate cardiac hypertrophy by suppressing autophagy. Proceedings of the National Academy of Sciences of the United States of America, 2011, 108: pp. 4123-4128.","DOI":"10.1073\/pnas.1015081108"},{"key":"ref51","doi-asserted-by":"publisher","unstructured":"Baran\u010d\u00edk M, Gre\u0161ov\u00e1 L, Bartekov\u00e1 M, Dovinov\u00e1 I. Nrf2 as a key player of redox regulation in cardiovascular diseases. Physiological Research, 2016, 65 Suppl 1: pp. S1-S10.","DOI":"10.33549\/physiolres.933403"},{"key":"ref52","doi-asserted-by":"publisher","unstructured":"Cuadrado A, Rojo AI, Wells G, Hayes JD, Cousin SP, Rumsey WL, et al. Therapeutic targeting of the NRF2 and KEAP1 partnership in chronic diseases. Nature Reviews. Drug Discovery, 2019, 18: pp. 295-317.","DOI":"10.1038\/s41573-018-0008-x"},{"key":"ref53","doi-asserted-by":"publisher","unstructured":"Liu T, Lv YF, Zhao JL, You QD, Jiang ZY. Regulation of Nrf2 by phosphorylation: Consequences for biological function and therapeutic implications. Free Radical Biology & Medicine, 2021, 168: pp. 129-141.","DOI":"10.1016\/j.freeradbiomed.2021.03.034"},{"key":"ref54","doi-asserted-by":"publisher","unstructured":"Kawai Y, Gardu\u00f1o L, Theodore M, Yang J, Arinze IJ. Acetylation-deacetylation of the transcription factor Nrf2 (nuclear factor erythroid 2-related factor 2) regulates its transcriptional activity and nucleocytoplasmic localization. The Journal of Biological Chemistry, 2011, 286: pp. 7629-7640.","DOI":"10.1074\/jbc.M110.208173"},{"key":"ref55","doi-asserted-by":"publisher","unstructured":"To KKW, Tolu SS, Wang L, Zhang H, Cho WC, Bates SE. HDAC inhibitors: Cardiotoxicity and paradoxical cardioprotective effect in ischemia-reperfusion myocardiocyte injury. Seminars in Cancer Biology, 2025, 113: pp. 25-38.","DOI":"10.1016\/j.semcancer.2025.05.008"},{"key":"ref56","doi-asserted-by":"publisher","unstructured":"Li F, Hu Z, Huang Y, Zhan H. Dexmedetomidine ameliorates diabetic cardiomyopathy by inhibiting ferroptosis through the Nrf2\/GPX4 pathway. Journal of Cardiothoracic Surgery, 2023, 18: pp. 223.","DOI":"10.1186\/s13019-023-02300-7"},{"key":"ref57","doi-asserted-by":"publisher","unstructured":"Mei SL, Xia ZY, Qiu Z, Jia YF, Zhou JJ, Zhou B. Shenmai Injection Attenuates Myocardial Ischemia\/Reperfusion Injury by Targeting Nrf2\/GPX4 Signalling-Mediated Ferroptosis. Chinese Journal of Integrative Medicine, 2022, 28: pp. 983-991.","DOI":"10.1007\/s11655-022-3620-x"},{"key":"ref58","doi-asserted-by":"publisher","unstructured":"Wang J, Ishfaq M, Fan Q, Chen C, Li J. 7-Hydroxycoumarin Attenuates Colistin-Induced Kidney Injury in Mice Through the Decreased Level of Histone Deacetylase 1 and the Activation of Nrf2 Signaling Pathway. Frontiers in Pharmacology, 2020, 11: pp. 1146.","DOI":"10.3389\/fphar.2020.01146"}],"container-title":["Die Pharmazie"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.imrpress.com\/journal\/Pharmazie\/81\/5\/10.31083\/Pharmazie51659","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T08:35:37Z","timestamp":1780130137000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.imrpress.com\/journal\/Pharmazie\/81\/5\/10.31083\/Pharmazie51659"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2026,5,28]]},"references-count":58,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2026]]}},"alternative-id":["S0031-7144(26)02943-0"],"URL":"https:\/\/doi.org\/10.31083\/pharmazie51659","relation":{},"ISSN":["0031-7144","3053-691X"],"issn-type":[{"value":"0031-7144","type":"print"},{"value":"3053-691X","type":"electronic"}],"subject":[],"published":{"date-parts":[[2026,5,28]]},"article-number":"51659"}}