心脏细胞衰老与Uvrag基因的缺失(5) - 心脏杂志杂志社投稿_期刊论文发表|版面费|电话|编辑部- 心脏杂志

一、本刊要求作者有严谨的学风和朴实的文风，提倡互相尊重和自由讨论。凡采用他人学说，必须加注说明。二、不要超过10000字为宜，精粹的短篇，尤为欢迎。三、请作者将稿件（用WORD格式）发送到下面给出的征文信箱中。四、凡来稿请作者自留底稿，恕不退稿。五、为规范排版，请作者在上传修改稿时严格按以下要求： 1．论文要求有题名、摘要、关键词、作者姓名、作者工作单位（名称，省市邮编）等内容一份。 2．基金项目和作者简介按下列格式：基金项目：项目名称（编号）作者简介：姓名（出生年－），性别，民族（汉族可省略），籍贯，职称，学位，研究方向。 3．文章一般有引言部分和正文部分，正文部分用阿拉伯数字分级编号法，一般用两级。插图下方应注明图序和图名。表格应采用三线表，表格上方应注明表序和表名。 4．参考文献列出的一般应限于作者直接阅读过的、最主要的、发表在正式出版物上的文献。其他相关注释可用脚注在当页标注。参考文献的著录应执行国家标准GB7714-87的规定，采用顺序编码制。

心脏细胞衰老与Uvrag基因的缺失(5)

作者:

关键词:

摘要：

文章查重：文章出版前已经过专业反剽窃文献检测系统进行3次查重。

文章外审：文章经小同行外审专家双盲外审，同行评议认为文章符合期刊发稿宗旨。

文章版权：文章出版前杂志已与全体作者授权人签署了版权相关协议。

开放获取声明：这是一篇开放获取文章，根据《知识共享许可协议》“署名-非商业性使用-相同方式共享4.0”条款，在合理引用的情况下，允许他人以非商业性目的基于原文内容编辑、调整和扩展，同时允许任何用户阅读、下载、拷贝、传递、打印、检索、超级链接该文献，并为之建立索引，用作软件的输入数据或其它任何合法用途。

4 参考文献 References

[1]DE ALMEIDA AJPO, RIBEIRO TP, DE MEDEIROS IA. Aging: molecular pathways and implications on the cardiovascular system. Oxid Med Cell Longev. 2017;2017:.

[2]CALCINOTTO A, KOHLI J, ZAGATO E, et al. Cellular senescence: aging, cancer,and Rev. 2019;99:1047-1078.

[3]ABATE M, FESTA A, FALCO M, et al. Mitochondria as playmakers of apoptosis,autophagy and senescence. Semin Cell Dev Biol. 2020;98:139-153.

[4]KOROLCHUK VI, MIWA S, CARROLL B, et al. Mitochondria in Cell Senescence:Is mitophagy the weakest link? ;21:7-13.

[5]REGULSKI MJ. Cellular Senescence: what, why, and how. Wounds. 2017;29:168-174.

[6]MARUSYK A, WHEELER LJ, MATHEWS CK, et al. p53 mediates senescencelike arrest induced by chronic replicational Cell Biol. 2007;27:5336-5351.

[7]RAYESS H, WANG MB, SRIVATSAN ES. Cellular senescence and tumor suppressor gene p16. Int J Cancer. 2012;130:1715-1725.

[8]KONG Y, CUI H, RAMKUMAR C, et of senescence in cancer and aging. J Aging Res. 2011;2011:.

[9]STORER M, MAS A, ROBERT-MORENO A, et al. Senescence is a developmental mechanism that contributes to embryonic growth and patterning. Cell. 2013;155:1119-1130.

[10]DA SILVA-áLVAREZ S, PICALLOS-RABINA P, ANTELO-IGLESIAS L, et al. The development of cell senescence. Exp Gerontol. 2019;128:.

[11]DA SILVA-áLVAREZ S, GUERRA-VARELA J, SOBRIDO-CAMEáN D, et al. Cell senescence contributes to tissue regeneration in zebrafish. Aging ;19:e.

[12]YUN MH. Cellular senescence in tissue repair: every cloud has a silver J Dev Biol. 2018;62:591-604.

[13]XU M, PIRTSKHALAVA T, FARR JN, et al. Senolytics improve physical function and increase lifespan in old age.Nat Med. 2018;24:1246-1256.

[14]CAMPISI J, KAPAHI P, LITHGOW GJ, et al. From discoveries in ageing research to therapeutics for healthy ageing. Nature. 2019;571:183-192.

[15]SHIMIZU I, MINAMINO T. Cellular senescence in cardiac ;74:313-319.

[16]MAVROGONATOU E, PRATSINIS H, KLETSAS D. The role of senescence in cancer development. Semin Cancer Biol. 2020;62:182-191.

[17]KRITSILIS M, V RIZOU S, KOUTSOUDAKI PN, et al. Ageing, Cellular Senescence and Neurodegenerative Disease. Int J Mol Sci. 2018;19. pii: E2937.

[18]SCHAFER MJ, HAAK AJ, TSCHUMPERLIN DJ, et al. Targeting senescent cells in fibrosis: pathology, paradox, and practical considerations. Curr Rheumatol Rep. 2018;20:3.

[19]PALMER AK, XU M, ZHU Y, et al. Targeting senescent cells alleviates obesityinduced metabolic dysfunction. Aging Cell. 2019;18:e.

[20]YOUSEFZADEH MJ, ZHU Y, MCGOWAN SJ, et al. Fisetin is a senotherapeutic that extends health and lifespan. EBioMedicine. 2018;36:18-28.

[21]GONZALEZ-VALDES I, HIDALGO I, BUJARRABAL A, et al. Bmi1 limits dilated cardiomyopathy and heart failure by inhibiting cardiac Commun. 2015;6:6473.

[22]YOUNG AR, NARITA M, FERREIRA M, et mediates the mitotic senescence transition. Genes Dev. 2009;23:798-803.

[23]KWON Y, KIM JW, JEOUNG JA, et is pro-senescence when seen in close-up, but anti-senescence in Cells. 2017;40:607-612.

[24]GARCíA-PRAT L, MARTíNEZ-VICENTE M, PERDIGUERO E, et al. Autophagy maintains stemness by preventing senescence. Nature. 2016;529:37-42.

[25]TAI H, WANG Z, GONG H, et al. Autophagy impairment with lysosomal and mitochondrial dysfunction is an important characteristic of oxidative stressinduced senescence. Autophagy. 2017;13:99-113.

[26]PARK JT, LEE YS, CHO KA, et al. Adjustment of the lysosomal-mitochondrial axis for control of cellular Res Rev. 2018;47:176-182.

[27]ZHU H, HE L. Uvrag: A multifunctional protein with essential roles in the heart. J Cardiol Curr Res. 2014;1:00003.

[28]SONG Y, QUACH C, LIANG C. Uvrag in autophagy, inflammation, and 2020;16:387-388.

[29]SONG Z, AN L, YE Y, et al. Essential role for Uvrag in autophagy and maintenance of cardiac function. Cardiovasc Res. 2014;101:48-56.

[30]HUDGINS AD, TAZEARSLAN C, TARE A, et al. Age- and tissue-specific expression of senescence biomarkers in mice. Front Genet. 2018;9:59.

[31]ZI Z, SONG Z, ZHANG S, et al. Rubicon deficiency enhances cardiac autophagy and protects mice from lipopolysaccharide-induced lethality and reduction in stroke volume.J Cardiovasc Pharmacol. 2015;65:252-261.

文章来源：《心脏杂志》网址: http://www.xzzzzzs.cn/qikandaodu/2021/0128/327.html