[1]Kioka N, Ueda K, Amachi T. CAP/ponsin, ArgBP2: a novel adaptor protein family regulating cytoskeletal organization and signal transduction\[J\]. Cell Struct Funct, 2002, 27(1):1-7.
[2]Kioka N, Sakata S, Kawauchi T, et al. Vinexin: a novel Vinculinbinding protein with multiple SH3 domains enhances actin cytoskeletal organization[J]. J Cell Biol, 1999, 144(1):59-69.
[3]Valaperti A, Nishii M, Liu Y, et al. The adapter protein cCblassociated protein (CAP) protects from acute CVB3mediated myocarditis through stabilization of type Ⅰ interferon production and reduced cytotoxicity\[J\]. Basic Res Cardiol, 2014, 109(3):411.
[4]Wang B, Golemis EA, Kruh GD. ArgBP2, a multiple src homology 3 domaincontaining, Arg/Ablinteracting protein, is phosphorylated in vAbltransformed cells and localized in stress fibers and cardiocyte Zdisks\[J\]. J Biol Chem, 1997, 272(28):17542-17550.
[5]Ichikawa T, Kita M, Matsui TS. Vinexin family (SORBS) proteins play different roles in stiffnesssensing and contractile force generation\[J\]. J Cell Sci, 2017, 130(20):3517-3531.
[6]Packer M. Longevity genes, cardiac ageing, and the pathogenesis of cardiomyopathy: implications for understanding the effects of current and future treatments for heart failure\[J\]. Eur Heart J, 2020.\[Epub ahead of print\]
[7]Bang C, Batkai S, Dangwal S, et al. Cardiac fibroblastderived microRNA passenger strandenriched exosomes mediate cardiomyocyte hypertrophy\[J\]. J Clin Invest, 2014, 124(5):2136-2146.
[8]Gan M, Zhang S, Zhang S, et al. The expression of microRNA in adult rat heart with isoproterenolinduced cardiac hypertrophy\[J\]. Cells, 2020, 9(5):E1173.
[9]Chen K, Gao L, Liu Y, et al.Vinexinβ protects against cardiac hypertrophy by blocking the Aktdependent signalling pathway\[J\]. Basic Res Cardiol, 2013, 108(2):338.
[10]Yan M, Chen C, Gong W, et al. miR213p regulates cardiac hypertrophic response by targeting histone deacetylase8\[J\]. Cardiovasc Res, 2015, 105(3):340-352.
[11]Wang H, Bei Y, Shen S, et al. miR213p controls sepsisassociated cardiac dysfunction via regulating SORBS2\[J\]. J Mol Cell Cardiol, 2016, 94:43-53.
[12]Abeyrathna P, Su Y. The critical role of Akt in cardiovascular function\[J\]. Vasc Pharmacol, 2015, 74:38-48.
[13]Shang L, Pin L, Zhu S, et al. Plantamajoside attenuates isoproterenolinduced cardiac hypertrophy associated with the HDAC2 and AKT/GSK3β signaling pathway\[J\]. Chem Biol Interact, 2019, 307:21-28.
[14]Shimizu I, Minamino T. Physiological and pathological cardiac hypertrophy\[J\]. J Mol Cell Cardiol, 2016, 97:245-262.
[15]Xin Z, Ma Z, Jiang S, et al. FOXOs in the impaired heart: New therapeutic targets for cardiac diseases\[J\]. Biochim Biophys Acta Mol Basis Dis, 2017, 1863(2):486-498.
[16]Kakimoto Y, Ito S, Abiru H, et al. Sorbin and SH3 domaincontaining protein 2 is released from infarcted heart in the very early phase: proteomic analysis of cardiac tissues from patients\[J\]. J Am Heart Assoc, 2013, 2(6):e000565.
[17]Liu X, Wan N, Zhang X, et al. Vinexinβ exacerbates cardiac dysfunction postmyocardial infarction via mediating apoptotic and inflammatory responses\[J\]. Clin Sci, 2015, 128(12):923-936.
[18]Pyle WG, Solaro RJ. At the crossroads of myocardial signaling: the role of ZDiscs in intracellular signaling and cardiacfunction\[J\]. Clin Sci, 2004, 94(3):296-305.
[19]Sanger JM, Wang J, Gleason LM, et al.Arg/Ablbinding protein, a Zbody and Zband protein, binds sarcomeric, costameric, and signaling molecules\[J\]. Cytoskeleton, 2010, 67(12):808-823.
[20]Rafiq K, Kolpakov MA, Seqqat R, et al. cCbl inhibition improves cardiac function and survival in response to myocardial ischemia\[J\]. Circulation, 2014, 129(20):2031-2043.
[21]Wang X, Guo Z, Ding Z, et al. Inflammation, autophagy, and apoptosis after myocardial infarction\[J\]. J Am Heart Assoc, 2018, 7(9):e008024.
[22]Wang X, Liu Y, Xiao L, et al. Hyperoside protects against pressure overloadinduced cardiac remodeling via the AKT signaling pathway\[J\]. Cell Physiol Biochem, 2018, 51(2):827-841.
[23]Chen BC, Hung MY, Wang HF, et al. GABA tea attenuates cardiac apoptosis in spontaneously hypertensive rats (SHR) by enhancing PI3K/Aktmediated survival pathway and suppressing Bax/Bak dependent apoptotic pathway\[J\]. Environ Toxicol, 2018, 33(7):789-797.
[24]Xia P, Liu Y, Cheng Z. Signaling pathways in cardiac myocyte apoptosis\[J\]. Biomed Res Int, 2016, 2016:9583268.
[25]阮中宝, 傅行礼, 李伟, 等. 靶向沉默Notch 1、2和3基因对动脉粥样硬化患者巨噬细胞Notch和核因子κB信号通路的影响\[J\]. 中华心血管病杂志, 2016, 44(9):786-792.
[26]Guan H, Cheng W, Guo J, et al. Vinexin β ablation inhibits atherosclerosis in apolipoprotein Edeficient mice by inactivating the Aktnuclear factor κB inflammatory axis\[J\]. J Am Heart Assoc, 2017, 6(2):e004585.
[27]Donners MM, Verluyten MJ, Bouwman FG, et al. Proteomic analysis of differential protein expression in human atherosclerotic plaque progression\[J\]. J Pathol, 2005, 206(1):39-45.
[28]Rotllan N, ChamorroJorganes A, Araldi E, et al. Hematopoietic Akt2 deficiency attenuates the progression of atherosclerosis\[J\]. FASEB J, 2015, 29(2):597-610.
[29]Gong Q, Li Y, Ma H, et al. Peiminine protects against lipopolysaccharideinduced mastitis by inhibiting the AKT/NFκB, ERK1/2 and p38 signaling pathways\[J\]. Int J Mol Sci, 2018, 19(9):2637.
[30]Wang JP, Cerny A, Asher DR, et al. MDA5 and MAVS mediate type Ⅰ interferon responses to coxsackie B virus\[J\]. J Virol, 2010, 84(1):254-260.
[31]Nelemans T, Kikkert M. Viral innate immune evasion and the pathogenesis of emerging RNA virus infections\[J\]. Viruses, 2019, 11(10):961.
[32]Li M, Su Y, Yu Y, et al. Dual roles of calpain in facilitating Coxsackievirus B3 replication and prompting inflammation in acute myocarditis\[J\]. Int J Cardiol, 2016, 221:1123-1131.
[33]Gebhard JR, Perry CM, Harkins S, et al. Coxsackievirus B3induced myocarditis: Perforin exacerbates disease, but plays no detectable role in virus clearance\[J\]. Am J Pathol, 1998, 153(2):417-428.
[34]Kato H, Takeuchi O, Sato S, et al. Differential roles of MDA5 and RIGI helicases in the recognition of RNA viruses\[J\]. Nature, 2006, 441(7089):101-105.
[35]Barral PM, Morrison JM, Drahos J, et al. MDA5 is cleaved in poliovirusinfected cells\[J\]. J Virol, 2007, 81(8):3677-3684.
[36]Kotla S, Gustin KE. Proteolysis of MDA5 and IPS1 is not required for inhibition of the type Ⅰ IFN response by poliovirus\[J\]. J Virol, 2015, 12:158.
[37]Xiang R, Chen J, Li S. VSMCspecific deletion of FAM3A attenuated AngⅡpromoted hypertension and cardiovascular hypertrophy\[J\]. Circ Res, 2020, 126(12):1746-1759.
[38]Mazzei L, Sanz R, Manucha W. Alterations on a key nephrogenic/cardiogenic gene expression linked to hypertension development\[J\]. Clin Investig Arterioscler, 2020, 32(2):70-78.
[39]Bigazzi R , Zagato L , Lanzani C , et al.Hypertension in high school students: genetic and environmental factors: the HYGEF study[J].Hypertension, 2020,75(1):71-78.
[40]Yamada Y, Ando F, Shimokata H. Association of polymorphisms of SORBS1, GCK and WISP1 with hypertension in communitydwelling Japanese individuals\[J\]. Hypertens Res, 2009, 32(5):325-331.
[41]Hagiwara N, Kitazono T, Kamouchi M, et al. Polymorphism in the sorbin and SH3domaincontaining1 (SORBS1) gene and the risk of brain infarction in the Japanese population: the Fukuoka Stroke Registry and the Hisayama study\[J\]. Eur J Neurol, 2008, 15: 481-486.
[42]Chang TJ, Wang WC, Hsiung CA, et al. Genetic variation in the human SORBS1 gene is associated with blood pressure regulation and age at onset of hypertension\[J\]. Medicine, 2016, 95(10):e2970.
[43]Lin H, Li Y, Zhu H, et al.Lansoprazole alleviates pressure overloadinduced cardiac hypertrophy and heart failure in mice by blocking the activation of βcatenin[J].Cardiovasc Res,2020,116(1):101-113.
[44]PadrónBarthe L, VillalbaOrero M, GómezSalinero JM, et al. Severe cardiac dysfunction and death caused by arrhythmogenic right ventricular cardiomyopathy type 5 are improved by inhibition of glycogen synthase kinase3β[J]. Circulation,2019,140(14):1188-1204.
[45]Chen MC, Chang JP, Lin YS, et al. Deciphering the gene expression profile of peroxisome proliferatoractivated receptor signaling pathway in the left atria of patients with mitral regurgitation\[J\]. J Transl Med, 2016, 14(1):157.
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