[1]刘贤玲 陈雪英 郭莹.细胞应激性衰老在心肌梗死中的作用及机制研究进展[J].心血管病学进展,2024,(5):416.[doi:10.16806/j.cnki.issn.1004-3934.2023.05.008]
 LIU Xianling,CHEN Xueying,GUO Ying..Role and Mechanism of Cell Senescence in Myocardial Infarction[J].Advances in Cardiovascular Diseases,2024,(5):416.[doi:10.16806/j.cnki.issn.1004-3934.2023.05.008]
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细胞应激性衰老在心肌梗死中的作用及机制研究进展()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2024年5期
页码:
416
栏目:
综述
出版日期:
2024-05-25

文章信息/Info

Title:
.Role and Mechanism of Cell Senescence in Myocardial Infarction
作者:
刘贤玲 1 陈雪英 2 郭莹 2
(1.济宁医学院临床医学院,山东 济宁 272000;2.济宁医学院附属医院心内科,山东 济宁 272000)
Author(s):
LIU Xianling1CHEN Xueying2GUO Ying2
?1.Clinical Medical School,Jining Medical University,Jining 272000 ,Sandong,China; 2. Department of Cardiology,Affiliated Hospital of Jining Medical University,Jining 272000,Sandong,China)
关键词:
细胞衰老衰老相关分泌表型心肌梗死药物治疗
Keywords:
Cell senescenceSenesence-associated secretory phenotypeMyocardial infarction Drug treatment
DOI:
10.16806/j.cnki.issn.1004-3934.2023.05.008
摘要:
细胞衰老被定义为不可逆的细胞周期停滞,其特征在于基因和蛋白质表达的显著改变以及衰老相关分泌表型的产生。心肌梗死后的心肌中血流需求和供应之间严重失衡可导致细胞应激性衰老的发生,其在决定心肌梗死后心脏功能转归中发挥重要作用。现主要对细胞应激性衰老在心肌梗死后维持心脏功能中的作用及机制,以及针对细胞衰老开发的药物对心肌梗死后心脏功能的影响等进行综述,为通过调节细胞衰老而改善心肌梗死的治疗提供一些新的思路。
Abstract:
Cell senescence is defined as irreversible cell cycle arrest characterized by significant alterations in gene and protein expression and the production of senesence-associated secretory phenotype. A severe imbalance between blood flow demand and supply in the myocardium after myocardial infarction can lead to the occurrence of stress cell senescence,which plays an important role in determining cardiac function outcomes after myocardial infarction. This article mainly reviews the role and mechanism of stress cell senescence in maintaining cardiac function in myocardial infarction,as well as the effect of drugs developed for cell senescence on cardiac function after myocardial infarction,so as to provide some new ideas for the treatment of myocardial infarction by regulating cellular senescence.

参考文献/References:

[1] Toldo S,Abbate A. The NLRP3 inflammasome in acute myocardial infarction[J]. Nat Rev Cardiol,2018,15(4):203-214.

[2] Calcinotto A,Kohli J,Zagato E,et al. Cellular senescence:aging,cancer,and injury[J]. Physiol Rev,2019,99(2):1047-1078.

[3] Luo X,Zhou J,Wang Z,et al. An inhibitor role of Nrf2 in the regulation of myocardial senescence and dysfunction after myocardial infarction[J]. Life Sci,2020,259:118199.

[4] Tang X,Li PH,Chen HZ. Cardiomyocyte senescence and cellular communications within myocardial microenvironments[J]. Front Endocrinol (Lausanne),2020, 21,11:280.

[5] Vujic A,Natarajan N,Lee RT. Molecular mechanisms of heart regeneration[J]. Semin Cell Dev Biol,2020,100:20-28.

[6] Chen MS,Lee RT,Garbern JC. Senescence mechanisms and targets in the heart[J]. Cardiovasc Res,2022,118(5):1173-1187.

[7] Karra R,Poss KD. Redirecting cardiac growth mechanisms for therapeutic regeneration[J]. J Clin Invest,2017,127(2):427-436.

[8] Saucerman JJ,Tan PM,Buchholz KS,et al. Mechanical regulation of gene expression in cardiac myocytes and fibroblasts[J]. Nat Rev Cardiol,2019,16(6):361-378.

[9] Daseke MJ 2nd,Tenkorang MAA,Chalise U,et al. Cardiac fibroblast activation during myocardial infarction wound healing:Fibroblast polarization after MI[J]. Matrix Biol,2020,91-92:109-116.

[10] López-Antona I,Contreras-Jurado C,Luque-Martín L,et al. Dynamic regulation of myofibroblast phenotype in cellular senescence[J]. Aging Cell,2022,21(4):e13580.

[11] Zhang Z,Shayani G,Xu Y,et al. Induction of senescence by loss of gata4 in cardiac fibroblasts[J]. Cells,2023,12(12):1652.

[12] Ishida T,Ishida M,Tashiro S,et al. DNA damage and senescence-associated inflammation in cardiovascular disease[J]. Biol Pharm Bull,2019,42(4):531-537.

[13] Cui S,Xue L,Yang F,et al. Postinfarction hearts are protected by premature senescent cardiomyocytes via GATA 4-dependent CCN 1 secretion[J]. J Am Heart Assoc,2018,7(18):e009111.

[14] Lyu G,Guan Y,Zhang C,et al. TGF-β signaling alters H4K20me3 status via miR-29 and contributes to cellular senescence and cardiac aging[J]. Nat Commun,2018,9(1):2560.

[15] Dookun E,Walaszczyk A,Redgrave R,et al. Clearance of senescent cells during cardiac ischemia-reperfusion injury improves recovery[J]. Aging Cell,2020,19(10):e13249.

[16] Zhang L,Pitcher LE,Yousefzadeh MJ,et al. Cellular senescence:a key therapeutic target in aging and diseases[J]. J Clin Invest,2022,132(15):e158450.

[17] Shekhova E. Mitochondrial reactive oxygen species as major effectors of antimicrobial immunity[J]. PLoS Pathog, 2020,16(5):e1008470.

[18] Yan C,Xu Z,Huang W. Cellular senescence affects cardiac regeneration and repair in ischemic heart disease[J]. Aging Dis,2021,12(2):552-569.

[19] Anderson R,Lagnado A,Maggiorani D,et al. Length-independent telomere damage drives post-mitotic cardiomyocyte senescence[J]. EMBO J,2019,38(5):e100492.

[20] Abdellatif M,Rainer PP,Sedej S,et al. Hallmarks of cardiovascular ageing[J]. Nat Rev Cardiol,2023,20(11):754-777.

[21] 师莹,赵莉莉,秦勤. 细胞衰老:心脏疾病治疗新思路[J]. 中国分子心脏病学杂志,2022,22(3):4725-4730.

[22] Gao Y,Hu Y,Liu Q,et al. Two-dimensional design strategy to construct smart fluorescent probes for the precise tracking of senescence[J]. Angew Chem Int Ed Engl,2021,60(19):10756-10765.

[23] Kirkland JL,Tchkonia T. Senolytic drugs:from discovery to translation[J]. J Intern Med,2020,288(5):518-536.

[24] Saccon TD,Nagpal R,Yadav H,et al. Senolytic combination of dasatinib and quercetin alleviates intestinal senescence and inflammation and modulates the gut microbiome in aged mice[J]. J Gerontol A Biol Sci Med Sci,2021,76(11):1895-1905.

[25] Walaszczyk A,Dookun E,Redgrave R,et al. Pharmacological clearance of senescent cells improves survival and recovery in aged mice following acute myocardial infarction[J]. Aging Cell,2019,18(3):e12945.

[26] Jia K,Dai Y,Liu A,et al. Senolytic agent navitoclax inhibits angiotensin II-induced heart failure in mice[J]. J Cardiovasc Pharmacol,2020,76(4):452-460.

[27] Aman Y,Schmauck-Medina T,Hansen M,et al. Autophagy in healthy aging and disease[J]. Nat Aging,2021,1(8):634-650.

[28] Partridge L,Fuentealba M,Kennedy BK. The quest to slow ageing through drug discovery[J]. Nat Rev Drug Discov,2020,19(8):513-532.

[29] Pyo IS,Yun S,Yoon YE,et al. Mechanisms of aging and the preventive effects of resveratrol on age-related diseases[J]. Molecules,2020,25(20):4649.

[30] Zhou DD,Luo M,Huang SY,et al. Effects and mechanisms of resveratrol on aging and age-related diseases[J]. Oxid Med Cell Longev,2021,2021:9932218.

[31] Breuss JM,Atanasov AG,Uhrin P. Resveratrol and its effects on the vascular system[J]. Int J Mol Sci,2019,20(7):1523.

[32] Chen H,Lou L,Zhang D,et al. Qiliqiangxin capsule improves cardiac function and attenuates cardiac remodeling by upregulating miR-133a after myocardial infarction in rats[J]. Evid Based Complement Alternat Med,2019,2019:7528214.

[33] Kang C. Senolytics and senostatics:a two-pronged approach to target cellular senescence for delaying aging and age-related diseases[J]. Mol Cells,2019,42(12):821-827.

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更新日期/Last Update: 2024-06-28