| [1] | Weiss A, Leinwand LA. The mammalian myosin heavy chain gene family. Annu Rev Cell Dev Biol, 1996; 12, 417−39. doi: 10.1146/annurev.cellbio.12.1.417 |
| [2] | Martin AA, Thompson BR, Hahn D, et al. Cardiac sarcomere signaling in health and disease. Int J Mol Sci, 2022; 23, 16223. doi: 10.3390/ijms232416223 |
| [3] | Gordon AM, Homsher E, Regnier M. Regulation of contraction in striated muscle. Physiol Rev, 2000; 80, 853−924. doi: 10.1152/physrev.2000.80.2.853 |
| [4] | Sun LJ, Li F, Tan WH, et al. Lithocholic acid promotes skeletal muscle regeneration through the TGR5 receptor. Acta Biochim Biophys Sin, 2023; 55, 51−61. |
| [5] | Markel TA, Wairiuko GM, Lahm T, et al. The right heart and its distinct mechanisms of development, function, and failure. J Surg Res, 2008; 146, 304−13. doi: 10.1016/j.jss.2007.04.003 |
| [6] | Malmqvist UP, Aronshtam A, Lowey S. Cardiac myosin isoforms from different species have unique enzymatic and mechanical properties. Biochemistry, 2004; 43, 15058−65. doi: 10.1021/bi0495329 |
| [7] | Miyata S, Minobe W, Bristow MR, et al. Myosin heavy chain isoform expression in the failing and nonfailing human heart. Circ Res, 2000; 86, 386−90. doi: 10.1161/01.RES.86.4.386 |
| [8] | Walklate J, Ferrantini C, Johnson CA, et al. Alpha and beta myosin isoforms and human atrial and ventricular contraction. Cell Mol Life Sci, 2021; 78, 7309−37. doi: 10.1007/s00018-021-03971-y |
| [9] | Carrier L, Mearini G, Stathopoulou K, et al. Cardiac myosin-binding protein C (MYBPC3) in cardiac pathophysiology. Gene, 2015; 573, 188−97. doi: 10.1016/j.gene.2015.09.008 |
| [10] | Carrier L, Bonne G, Bahrend E, et al. Organization and sequence of human cardiac myosin binding protein C gene (MYBPC3) and identification of mutations predicted to produce truncated proteins in familial hypertrophic cardiomyopathy. Circ Res, 1997; 80, 427−34. doi: 10.1161/01.res.0000435859.24609.b3 |
| [11] | Marian AJ. Molecular genetic basis of hypertrophic cardiomyopathy. Circ Res, 2021; 128, 1533−53. doi: 10.1161/CIRCRESAHA.121.318346 |
| [12] | Chung H, Kim Y, Park CH, et al. Contribution of sarcomere gene mutations to left atrial function in patients with hypertrophic cardiomyopathy. Cardiovasc Ultrasound, 2021; 19, 4. doi: 10.1186/s12947-020-00233-y |
| [13] | Marian AJ, Braunwald E. Hypertrophic cardiomyopathy: genetics, pathogenesis, clinical manifestations, diagnosis, and therapy. Circ Res, 2017; 121, 749−70. doi: 10.1161/CIRCRESAHA.117.311059 |
| [14] | Girolami F, Ho CY, Semsarian C, et al. Clinical features and outcome of hypertrophic cardiomyopathy associated with triple sarcomere protein gene mutations. J Am Coll Cardiol, 2010; 55, 1444−53. doi: 10.1016/j.jacc.2009.11.062 |
| [15] | Geisterfer-Lowrance AAT, Kass S, Tanigawa G, et al. A molecular basis for familial hypertrophic cardiomyopathy: a β cardiac myosin heavy chain gene missense mutation. Cell, 1990; 62, 999−1006. doi: 10.1016/0092-8674(90)90274-I |
| [16] | Hodatsu A, Konno T, Hayashi K, et al. Compound heterozygosity deteriorates phenotypes of hypertrophic cardiomyopathy with founder MYBPC3 mutation: evidence from patients and zebrafish models. Am J Physiol Heart Circ Physiol, 2014; 307, H1594−604. doi: 10.1152/ajpheart.00637.2013 |
| [17] | Saltzman AJ, Mancini-DiNardo D, Li CM, et al. Short Communication: the cardiac myosin binding protein C Arg502Trp mutation: a common cause of hypertrophic cardiomyopathy. Circ Res, 2010; 106, 1549−52. doi: 10.1161/CIRCRESAHA.109.216291 |
| [18] | Capek P, Vondrasek J, Skvor J, et al. Hypertrophic cardiomyopathy: from mutation to functional analysis of defective protein. Croat Med J, 2011; 52, 384−91. doi: 10.3325/cmj.2011.52.384 |
| [19] | Purushotham G, Madhumohan K, Anwaruddin M, et al. The MYH7 p. R787H mutation causes hypertrophic cardiomyopathy in two unrelated families. Exp Clin Cardiol, 2010; 15, e1−4. |
| [20] | Hougs L, Havndrup O, Bundgaard H, et al. One third of Danish hypertrophic cardiomyopathy patients have mutations in MYH7 rod region. Eur J Hum Genet, 2005; 13, 161−5. doi: 10.1038/sj.ejhg.5201310 |
| [21] | Wang B, Wang J, Wang LF, et al. Genetic analysis of monoallelic double MYH7 mutations responsible for familial hypertrophic cardiomyopathy. Mol Med Rep, 2019; 20, 5229−38. |
| [22] | Erdmann J, Daehmlow S, Wischke S, et al. Mutation spectrum in a large cohort of unrelated consecutive patients with hypertrophic cardiomyopathy. Clin Genet, 2003; 64, 339−49. doi: 10.1034/j.1399-0004.2003.00151.x |
| [23] | Richard P, Charron P, Carrier L, et al. Hypertrophic cardiomyopathy: distribution of disease genes, spectrum of mutations, and implications for a molecular diagnosis strategy. Circulation, 2003; 107, 2227−32. doi: 10.1161/01.CIR.0000066323.15244.54 |
| [24] | Kimura A, Harada H, Park JE, et al. Mutations in the cardiac troponin I gene associated with hypertrophic cardiomyopathy. Nat Genet, 1997; 16, 379−82. doi: 10.1038/ng0897-379 |
| [25] | Thierfelder L, Watkins H, MacRae C, et al. α-tropomyosin and cardiac troponin T mutations cause familial hypertrophic cardiomyopathy: a disease of the sarcomere. Cell, 1994; 77, 701−12. doi: 10.1016/0092-8674(94)90054-X |
| [26] | Millat G, Bouvagnet P, Chevalier P, et al. Prevalence and spectrum of mutations in a cohort of 192 unrelated patients with hypertrophic cardiomyopathy. Eur J Med Genet, 2010; 53, 261−7. doi: 10.1016/j.ejmg.2010.07.007 |
| [27] | Marian AJ. The case of “missing causal genes” and the practice of medicine: a Sherlock Holmes approach of deductive reasoning. Circ Res, 2016; 119, 21−4. doi: 10.1161/CIRCRESAHA.116.308830 |
| [28] | Maron BJ, Mathenge R, Casey SA, et al. Clinical profile of hypertrophic cardiomyopathy identified de novo in rural communities. J Am Coll Cardiol, 1999; 33, 1590−5. doi: 10.1016/S0735-1097(99)00039-X |
| [29] | Unverferth DV, Baker PB, Pearce LI, et al. Regional myocyte hypertrophy and increased interstitial myocardial fibrosis in hypertrophic cardiomyopathy. Am J Cardiol, 1987; 59, 932−6. doi: 10.1016/0002-9149(87)91128-3 |
| [30] | Sachdev B, Takenaka T, Teraguchi H, et al. Prevalence of anderson-fabry disease in male patients with late onset hypertrophic cardiomyopathy. Circulation, 2002; 105, 1407−11. doi: 10.1161/01.CIR.0000012626.81324.38 |
| [31] | Wu JQ, Xiao DR, Yu KW, et al. The protective effect of the mitochondrial-derived peptide MOTS-c on LPS-induced septic cardiomyopathy. Acta Biochim Biophys Sin, 2023; 55, 285−94. doi: 10.3724/abbs.2023006 |
| [32] | Chi HY, Chai YE, Ma LJ, et al. The mechanism by which piR-000699 targets SLC39A14 regulates ferroptosis in aging myocardial schemia/reperfusion injury. Acta Biochim Biophys Sin, 2024; 56, 1352−64. doi: 10.3724/abbs.2024024 |
| [33] | Seo J, Kim M, Hong GR, et al. Fabry disease in patients with hypertrophic cardiomyopathy: a practical approach to diagnosis. J Hum Genet, 2016; 61, 775−80. doi: 10.1038/jhg.2016.52 |
| [34] | Chimenti C, Pieroni M, Morgante E, et al. Prevalence of Fabry disease in female patients with late-onset hypertrophic cardiomyopathy. Circulation, 2004; 110, 1047−53. doi: 10.1161/01.CIR.0000139847.74101.03 |
| [35] | Ruiz-Guerrero L, Barriales-Villa R. Storage diseases with hypertrophic cardiomyopathy phenotype. Glob Cardiol Sci Pract, 2018; 2018, 28. |
| [36] | Arad M, Seidman JG, Seidman CE. Phenotypic diversity in hypertrophic cardiomyopathy. Hum Mol Genet, 2002; 11, 2499−506. doi: 10.1093/hmg/11.20.2499 |
| [37] | Platt FM, d’Azzo A, Davidson BL, et al. Lysosomal storage diseases. Nat Rev Dis Primers, 2018; 4, 27. doi: 10.1038/s41572-018-0025-4 |
| [38] | Marian AJ. Challenges in the diagnosis of Anderson-Fabry disease: a deceptively simple and yet complicated genetic disease. J Am Coll Cardiol, 2016; 68, 1051−3. doi: 10.1016/j.jacc.2016.06.026 |
| [39] | Yu KW, Su X, Zhou TF, et al. EEPD1 attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading FOXO3A in cardiomyocytes. Acta Biochim Biophys Sin, 2024; 56, 1733−47. doi: 10.3724/abbs.2024130 |
| [40] | Rong Y, Zhou X, Guo ZL, et al. Activation of Kir2.1 improves myocardial fibrosis by inhibiting Ca2+ overload and the TGF-β1/smad signaling pathway. Acta Biochim Biophys Sin, 2023; 55, 749−57. doi: 10.3724/abbs.2023083 |
| [41] | Xiong TH, Wang DH, Yang HP, et al. miR-194-3p regulates epithelial-mesenchymal transition in embryonic epicardial cells via p120/β-catenin signaling. Acta Biochim Biophys Sin, 2024; 56, 717−29. |
| [42] | Stefl S, Nishi H, Petukh M, et al. Molecular mechanisms of disease-causing missense mutations. J Mol Biol, 2013; 425, 3919−36. doi: 10.1016/j.jmb.2013.07.014 |
| [43] | Pearce A, Ponnam S, Holt MR, et al. Missense mutations in the central domains of cardiac myosin binding protein-C and their potential contribution to hypertrophic cardiomyopathy. J Biol Chem, 2024; 300, 105511. doi: 10.1016/j.jbc.2023.105511 |
| [44] | Marston S, Copeland ON, Gehmlich K, et al. How do MYBPC3 mutations cause hypertrophic cardiomyopathy? J Muscle Res Cell Motil, 2012; 33, 75-80. |
| [45] | Desai DA, Baby A, Ananthamohan K, et al. Roles of cMyBP-C phosphorylation on cardiac contractile dysfunction in db/db mice. J Mol Cell Cardiol Plus, 2024; 8, 100075. |
| [46] | Moss RL, Fitzsimons DP, Ralphe JC. Cardiac MyBP-C regulates the rate and force of contraction in mammalian myocardium. Circ Res, 2015; 116, 183−92. doi: 10.1161/CIRCRESAHA.116.300561 |
| [47] | Ponnam S, Kampourakis T. Microscale thermophoresis suggests a new model of regulation of cardiac myosin function via interaction with cardiac myosin-binding protein C. J Biol Chem, 2022; 298, 101485. doi: 10.1016/j.jbc.2021.101485 |
| [48] | Kao KY, Childers MC, Mohran S, et al. A molecular scale investigation of the mechanisms of contractile dysfunction for the hypertrophic cardiomyopathy MYH7 G256E mutation. Biophys J, 2023; 122, 402A. |
| [49] | Kingdom R, Wright CF. Incomplete penetrance and variable expressivity: from clinical studies to population cohorts. Front Genet, 2022; 13, 920390. doi: 10.3389/fgene.2022.920390 |
| [50] | Lee S, Vander Roest AS, Blair CA, et al. Incomplete-penetrant hypertrophic cardiomyopathy MYH7 G256E mutation causes hypercontractility and elevated mitochondrial respiration. Proc Natl Acad Sci USA, 2024; 121, e2318413121. doi: 10.1073/pnas.2318413121 |
| [51] | Pan GP, Cui BY, Han MM, et al. Puerarin inhibits NHE1 activity by interfering with the p38 pathway and attenuates mitochondrial damage induced by myocardial calcium overload in heart failure rats. Acta Biochim Biophys Sin, 2024; 56, 270−9. doi: 10.3724/abbs.2023269 |
| [52] | Ranjbarvaziri S, Kooiker KB, Ellenberger M, et al. Altered cardiac energetics and mitochondrial dysfunction in hypertrophic cardiomyopathy. Circulation, 2021; 144, 1714−31. doi: 10.1161/CIRCULATIONAHA.121.053575 |
| [53] | Nollet EE, Duursma I, Rozenbaum A, et al. Mitochondrial dysfunction in human hypertrophic cardiomyopathy is linked to cardiomyocyte architecture disruption and corrected by improving NADH-driven mitochondrial respiration. Eur Heart J, 2023; 44, 1170−85. doi: 10.1093/eurheartj/ehad028 |
| [54] | Rosca MG, Tandler B, Hoppel CL. Mitochondria in cardiac hypertrophy and heart failure. J Mol Cell Cardiol, 2013; 55, 31−41. doi: 10.1016/j.yjmcc.2012.09.002 |
| [55] | da Silva Menezes Junior A, de França-e-Silva ALG, de Oliveira HL, et al. Genetic mutations and mitochondrial redox signaling as modulating factors in hypertrophic cardiomyopathy: a scoping review. Int J Mol Sci, 2024; 25, 5855. doi: 10.3390/ijms25115855 |
| [56] | Fang CX, Dong F, Thomas DP, et al. Hypertrophic cardiomyopathy in high-fat diet-induced obesity: role of suppression of forkhead transcription factor and atrophy gene transcription. Am J Physiol Heart Circ Physiol, 2008; 295, H1206−15. doi: 10.1152/ajpheart.00319.2008 |
| [57] | Huang WJ, Zhou R, Jiang CS, et al. Mitochondrial dysfunction is associated with hypertrophic cardiomyopathy in pompe disease‐specific induced pluripotent stem cell‐derived cardiomyocytes. Cell Proliferation, 2024; 57, e13573. doi: 10.1111/cpr.13573 |
| [58] | Yang D, Liu HQ, Liu FY, et al. Mitochondria in pathological cardiac hypertrophy research and therapy. Front Cardiovasc Med, 2022; 8, 822969. doi: 10.3389/fcvm.2021.822969 |
| [59] | Facundo HDTF, Brainard RE, de Lemos Caldas FR, et al. Mitochondria and cardiac hypertrophy. In: Information A. Mitochondrial Dynamics in Cardiovascular Medicine. Springer. 2017, 203-26. |
| [60] | Osterholt M, Nguyen TD, Schwarzer M, et al. Alterations in mitochondrial function in cardiac hypertrophy and heart failure. Heart Fail Rev, 2013; 18, 645−56. doi: 10.1007/s10741-012-9346-7 |
| [61] | Tokuyama T, Yanagi S. Role of mitochondrial dynamics in heart diseases. Genes, 2023; 14, 1876. doi: 10.3390/genes14101876 |
| [62] | Armstrong JS. Mitochondrial medicine: pharmacological targeting of mitochondria in disease. Br J Pharmacol, 2007; 151, 1154−65. doi: 10.1038/sj.bjp.0707288 |
| [63] | Viscomi C, Zeviani M. Strategies for fighting mitochondrial diseases. J Intern Med, 2020; 287, 665−84. doi: 10.1111/joim.13046 |
| [64] | Li QY, Huang Y. Mitochondrial targeted strategies and their application for cancer and other diseases treatment. J Pharm Investig, 2020; 50, 271−93. doi: 10.1007/s40005-020-00481-0 |
| [65] | Huang XY, Zeng ZH, Li SQ, et al. The therapeutic strategies targeting mitochondrial metabolism in cardiovascular disease. Pharmaceutics, 2022; 14, 2760. doi: 10.3390/pharmaceutics14122760 |
| [66] | Bonora M, Wieckowski MR, Sinclair DA, et al. Targeting mitochondria for cardiovascular disorders: therapeutic potential and obstacles. Nat Rev Cardiol, 2019; 16, 33−55. doi: 10.1038/s41569-018-0074-0 |
| [67] | Khalilimeybodi A, Saucerman JJ, Rangamani P. Modeling cardiomyocyte signaling and metabolism predicts genotype-to-phenotype mechanisms in hypertrophic cardiomyopathy. Comput Biol Med, 2024; 175, 108499. doi: 10.1016/j.compbiomed.2024.108499 |
| [68] | Yan Z, Liu YF, Yang BW, et al. Endoplasmic reticulum stress caused by traumatic injury promotes cardiomyocyte apoptosis through acetylation modification of GRP78. Acta Biochim Biophys Sin, 2024; 56, 96−105. doi: 10.3724/abbs.2023277 |
| [69] | Tian DY, Meng JQ, Li L, et al. Hydrogen sulfide ameliorates senescence in vascular endothelial cells through ameliorating inflammation and activating PPARδ/SGLT2/STAT3 signaling pathway. Acta Biochim Biophys Sin, 2023; 55, 1358−69. |
| [70] | Sun XT, Zhou Q, Xiao CP, et al. Role of post-translational modifications of Sp1 in cardiovascular diseases. Front Cell Dev Biol, 2024; 12, 1453901. doi: 10.3389/fcell.2024.1453901 |
| [71] | Ding J, Fayyaz AI, Ding YC, et al. Role of specificity protein 1 (SP1) in cardiovascular diseases: pathological mechanisms and therapeutic potentials. Biomolecules, 2024; 14, 807. doi: 10.3390/biom14070807 |
| [72] | Sack MN, Disch DL, Rockman HA, et al. A role for Sp and nuclear receptor transcription factors in a cardiac hypertrophic growth program. Proc Natl Acad Sci USA, 1997; 94, 6438−43. doi: 10.1073/pnas.94.12.6438 |
| [73] | Takizawa T, Arai M, Tomaru K, et al. Transcription factor Sp1 regulates SERCA2 gene expression in pressure-overloaded hearts: a study using in vivo direct gene transfer into living myocardium. J Mol Cell Cardiol, 2003; 35, 777−83. doi: 10.1016/S0022-2828(03)00122-6 |
| [74] | Zhang FL, Zhou HX, Xue JF, et al. Deficiency of transcription factor Sp1 contributes to hypertrophic cardiomyopathy. Circ Res, 2024; 134, 290−306. doi: 10.1161/CIRCRESAHA.123.323272 |
| [75] | Azakie A, Fineman JR, He YP. Sp3 inhibits Sp1-mediated activation of the cardiac troponin T promoter and is downregulated during pathological cardiac hypertrophy in vivo. Am J Physiol Heart Circ Physiol, 2006; 291, H600−11. doi: 10.1152/ajpheart.01305.2005 |
| [76] | Shichiri M, Ishimaru S, Ota T, et al. Salusins: newly identified bioactive peptides with hemodynamic and mitogenic activities. Nat Med, 2003; 9, 1166−72. doi: 10.1038/nm913 |
| [77] | Arkan A, Atukeren P, Ikitimur B, et al. The importance of circulating levels of salusin-α, salusin-β, and heregulin-β1 in atherosclerotic coronary arterial disease. Clin Biochem, 2021; 87, 19−25. doi: 10.1016/j.clinbiochem.2020.10.003 |
| [78] | Suzuki N, Shichiri M, Akashi T, et al. Systemic distribution of salusin expression in the rat. Hypertens Res, 2007; 30, 1255−62. doi: 10.1291/hypres.30.1255 |
| [79] | Suzuki N, Shichiri M, Tateno T, et al. Distinct systemic distribution of salusin-α and salusin-β in the rat. Peptides, 2011; 32, 805−10. doi: 10.1016/j.peptides.2010.12.012 |
| [80] | Sato K, Koyama T, Tateno T, et al. Presence of immunoreactive salusin-α in human serum and urine. Peptides, 2006; 27, 2561−6. doi: 10.1016/j.peptides.2006.06.005 |
| [81] | Sato K, Sato T, Susumu T, et al. Presence of immunoreactive salusin-β in human plasma and urine. Regul Pept, 2009; 158, 63−7. doi: 10.1016/j.regpep.2009.07.017 |
| [82] | Li CY, Liu R, Xiong ZY, et al. Ferroptosis: a potential target for the treatment of atherosclerosis. Acta Biochim Biophys Sin, 2024; 56, 331−44. |
| [83] | Watanabe T, Sato K, Itoh F, et al. The roles of salusins in atherosclerosis and related cardiovascular diseases. J Am Soc Hypertens, 2011; 5, 359−65. doi: 10.1016/j.jash.2011.06.003 |
| [84] | Li CY, Zhu XS, Chen JX, et al. Multifaceted role of ferroptosis in cardiovascular disease. Acta Biochim Biophys Sin, 2023; 55, 183−93. doi: 10.3724/abbs.2023019 |
| [85] | Yuan M, Ceylan AF, Gao RF, et al. Selective inhibition of the NLRP3 inflammasome protects against acute ethanol-induced cardiotoxicity in an FBXL2-dependent manner. Acta Biochim Biophys Sin, 2023; 55, 1972−86. doi: 10.3724/abbs.2023256 |
| [86] | Dang JY, Zhang W, Chu Y, et al. Downregulation of salusins alleviates hypertrophic cardiomyopathy via attenuating oxidative stress and autophagy. Eur J Med Res, 2024; 29, 109. doi: 10.1186/s40001-024-01676-z |
| [87] | Wang J, Li DX, Zhang Y, et al. Angiotensin II type 1a receptor knockout ameliorates high-fat diet-induced cardiac dysfunction by regulating glucose and lipid metabolism. Acta Biochim Biophys Sin, 2023; 55, 1380−92. |
| [88] | Frieler RA, Mortensen RM. Immune cell and other noncardiomyocyte regulation of cardiac hypertrophy and remodeling. Circulation, 2015; 131, 1019−30. doi: 10.1161/CIRCULATIONAHA.114.008788 |
| [89] | Zheng XF, Yang Y, Fu CH, et al. Identification and verification of promising diagnostic biomarkers in patients with hypertrophic cardiomyopathy associate with immune cell infiltration characteristics. Life Sci, 2021; 285, 119956. doi: 10.1016/j.lfs.2021.119956 |
| [90] | Gong JM, Shi B, Yang P, et al. Unveiling immune infiltration characterizing genes in hypertrophic cardiomyopathy through transcriptomics and bioinformatics. J Inflamm Res, 2024; 17, 3079−92. doi: 10.2147/JIR.S454446 |
| [91] | Zhang XZ, Zhang S, Tang TT, et al. Bioinformatics and immune infiltration analyses reveal the key pathway and immune cells in the pathogenesis of hypertrophic cardiomyopathy. Front Cardiovasc Med, 2021; 8, 696321. doi: 10.3389/fcvm.2021.696321 |
| [92] | Liu X, Shi GP, Guo JL. Innate immune cells in pressure overload-induced cardiac hypertrophy and remodeling. Front Cell Dev Biol, 2021; 9, 659666. doi: 10.3389/fcell.2021.659666 |
| [93] | Lillo R, Graziani F, Franceschi F, et al. Inflammation across the spectrum of hypertrophic cardiac phenotypes. Heart Fail Rev, 2023; 28, 1065−75. doi: 10.1007/s10741-023-10307-4 |
| [94] | Zhang C, Wang F, Zhang YX, et al. Celecoxib prevents pressure overload‐induced cardiac hypertrophy and dysfunction by inhibiting inflammation, apoptosis and oxidative stress. J Cell Mol Med, 2016; 20, 116−27. doi: 10.1111/jcmm.12709 |
| [95] | Kumar V, Prabhu SD, Bansal SS. CD4+ T-lymphocytes exhibit biphasic kinetics post-myocardial infarction. Front Cardiovasc Med, 2022; 9, 992653. doi: 10.3389/fcvm.2022.992653 |
| [96] | Rurik JG, Aghajanian H, Epstein JA. Immune cells and immunotherapy for cardiac injury and repair. Circ Res, 2021; 128, 1766−79. doi: 10.1161/CIRCRESAHA.121.318005 |
| [97] | Abplanalp WT, John D, Cremer S, et al. Single-cell RNA-sequencing reveals profound changes in circulating immune cells in patients with heart failure. Cardiovasc Res, 2021; 117, 484−94. doi: 10.1093/cvr/cvaa101 |
| [98] | Kumar V, Rosenzweig R, Asalla S, et al. TNFR1 contributes to activation-induced cell death of pathological CD4+ T lymphocytes during ischemic heart failure. JACC Basic Transl Sci, 2022; 7, 1038−49. doi: 10.1016/j.jacbts.2022.05.005 |
| [99] | Jablonka E, Lamb MJ. The changing concept of epigenetics. Ann N Y Acad Sci, 2002; 981, 82−96. doi: 10.1111/j.1749-6632.2002.tb04913.x |
| [100] | Shi YC, Zhang HJ, Huang SL, et al. Epigenetic regulation in cardiovascular disease: mechanisms and advances in clinical trials. Signal Transduct Target Ther, 2022; 7, 200. doi: 10.1038/s41392-022-01055-2 |
| [101] | Colpaert RMW, Calore M. Epigenetics and microRNAs in cardiovascular diseases. Genomics, 2021; 113, 540−51. doi: 10.1016/j.ygeno.2020.12.042 |
| [102] | Lei H, Hu JH, Sun KJ, et al. The role and molecular mechanism of epigenetics in cardiac hypertrophy. Heart Fail Rev, 2021; 26, 1505−14. doi: 10.1007/s10741-020-09959-3 |
| [103] | Han Y, Nie JL, Wang DW, et al. Mechanism of histone deacetylases in cardiac hypertrophy and its therapeutic inhibitors. Front Cardiovasc Med, 2022; 9, 931475. doi: 10.3389/fcvm.2022.931475 |
| [104] | Gilsbach R, Preissl S, Grüning BA, et al. Dynamic DNA methylation orchestrates cardiomyocyte development, maturation and disease. Nat Commun, 2014; 5, 5288. doi: 10.1038/ncomms6288 |
| [105] | Xiao DL, Dasgupta C, Chen M, et al. Inhibition of DNA methylation reverses norepinephrine-induced cardiac hypertrophy in rats. Cardiovasc Res, 2014; 101, 373−82. doi: 10.1093/cvr/cvt264 |
| [106] | Sasaki K, Hara S, Yamakami R, et al. Ectopic expression of DNA methyltransferases DNMT3A2 and DNMT3L leads to aberrant hypermethylation and postnatal lethality in mice. Mol Reprod Dev, 2019; 86, 614−23. doi: 10.1002/mrd.23137 |
| [107] | Liu CF, Tang WHW. Epigenetics in cardiac hypertrophy and heart failure. JACC Basic Transl Sci, 2019; 4, 976−93. doi: 10.1016/j.jacbts.2019.05.011 |
| [108] | Funamoto M, Imanishi M, Tsuchiya K, et al. Roles of histone acetylation sites in cardiac hypertrophy and heart failure. Front Cardiovasc Med, 2023; 10, 1133611. doi: 10.3389/fcvm.2023.1133611 |
| [109] | Papait R, Cattaneo P, Kunderfranco P, et al. Genome-wide analysis of histone marks identifying an epigenetic signature of promoters and enhancers underlying cardiac hypertrophy. Proc Natl Acad Sci USA, 2013; 110, 20164−9. doi: 10.1073/pnas.1315155110 |
| [110] | Kouzarides T. Histone methylation in transcriptional control. Curr Opin Genet Dev, 2002; 12, 198−209. doi: 10.1016/S0959-437X(02)00287-3 |
| [111] | Krauss V. Glimpses of evolution: heterochromatic histone H3K9 methyltransferases left its marks behind. Genetica, 2008; 133, 93−106. doi: 10.1007/s10709-007-9184-z |
| [112] | Nührenberg T, Gilsbach R, Preissl S, et al. Epigenetics in cardiac development, function, and disease. Cell Tissue Res, 2014; 356, 585−600. doi: 10.1007/s00441-014-1887-8 |