[1]程晓蔚 朱庆磊.线粒体ATP敏感钾通道线粒体自噬对心力衰竭的作用研究[J].心血管病学进展,2023,(2):163-166,171.[doi:10.16806/j.cnki.issn.1004-3934.2023.02.015]
 CHENG XiaoweiZHU Qinglei.The Role of Mitochondrial ATP-Sensitive Potassium Channel[J].Advances in Cardiovascular Diseases,2023,(2):163-166,171.[doi:10.16806/j.cnki.issn.1004-3934.2023.02.015]
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线粒体ATP敏感钾通道线粒体自噬对心力衰竭的作用研究()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2023年2期
页码:
163-166,171
栏目:
综述
出版日期:
2023-02-25

文章信息/Info

Title:
The Role of Mitochondrial ATP-Sensitive Potassium Channel
作者:
程晓蔚12 朱庆磊2
(1.解放军医学院,北京 100853;2. 解放军总医院第六医学中心心血管病医学部,北京 100853)
Author(s):
CHENG Xiaowei12ZHU Qinglei2
(1. Chinese?PLA?Medical?School,?Beijing?100853,?China2. Medical Department of Cardiovascular DiseaseThe Sixth Medical Center,Chinese PLA General Hospital,Beijing 100853,China)
关键词:
心力衰竭线粒体ATP敏感钾通道线粒体自噬
Keywords:
Heart failureMitochondrial ATP-sensitive potassium channelMitophagy
DOI:
10.16806/j.cnki.issn.1004-3934.2023.02.015
摘要:
心力衰竭是由心脏的收缩功能和或舒张功能发生障碍,导致心室泵血功能受损引起的循环障碍症候群。临床主要表现为呼吸困难、咳嗽和咳痰。心力衰竭是心脏疾病发展的终末阶段,患者预后较差,目前心力衰竭的发病机制尚不完全明确。近年来,许多研究表明线粒体功能障碍心力衰竭的发生发展密切相关。对线粒体ATP敏感钾通道以线粒体自噬对心力衰竭的作用进展进行综述。
Abstract:
Heart failure is a circulatory disorder syndrome caused by impairment of the systolic and/or diastolic function of the heartresulting in impaired ventricular pumping function. The main clinical manifestations are dyspnea,cough and sputum. Heart failure is the end stage of the development of heart disease with poor prognosis. Until now,the pathogenesis of heart failure is not fully clarified. In recent years,many studies have shown that mitochondrial dysfunction is closely related to the occurrence and development of heart failure. In this article,we reviewed the progress of mitochondrial ATP-sensitive potassium channels and the role of mitophagy in heart failure

参考文献/References:

[1] Heidenreich PABozkurt B,Aguilar D,et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure:A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines[J]. Circulation,2022,145(18):e895-e1032.
[2] Hao G,Wang X,Chen Z,et al. Prevalence of heart failure and left ventricular dysfunction in China:the China Hypertension Survey,2012-2015[J]. Eur J Heart Fail,2019,21(11):1329-1337.
[3] 中华医学会心血管病学分会心力衰竭学组中国医师协会心力衰竭专业委员会中华心血管病杂志编辑委员会. 中国心力衰竭诊断和治疗指南2018[J]. 中华心血管病杂志,2018,46(10):30.
[4] Noma A. ATP-regulated K+ channels in cardiac muscle[J]. Nature1983,305(5930):147-148.
[5] Inoue I,Nagase H,Kishi K,et al. ATP-sensitive K+ channel in the mitochondrial inner membrane[J]. Nature,1991,352(6332):244-247.
[6] Nichols CG,Singh GK,Grange DK. KATP channels and cardiovascular disease:suddenly a syndrome[J]. Circ Res,2013,112(7):1059-1072.
[7] Suzuki M,Kotake K,Fujikura K,et al. Kir6.1:a possible subunit of ATP-sensitive K+ channels in mitochondria[J]. Biochem Biophys Res Commun,1997,241(3):693-697.
[8] Liu Y,Ren G,O’Rourke B,et al. Pharmacological comparison of native mitochondrial K(ATP) channels with molecularly defined surface K(ATP) channels[J]. Mol Pharmacol,2001,59(2):225-230.
[9] Dos Santos P,Kowaltowski AJ,Laclau MN,et al. Mechanisms by which opening the mitochondrial ATP- sensitive K(+) channel protects the ischemic heart[J]. Am J Physiol Heart Circ Physiol,2002,283(1):H284-H295.
[10] Kowaltowski AJ,Seetharaman S,Paucek P,et al. Bioenergetic consequences of opening the ATP-sensitive K(+) channel of heart mitochondria[J]. Am J Physiol Heart Circ Physiol,2001,280(2):H649-H657.
[11] Garlid KD,Dos Santos P,Xie ZJ,et al. Mitochondrial potassium transport:the role of the mitochondrial ATP-sensitive K(+) channel in cardiac function and cardioprotection[J]. Biochim Biophys Acta,2003,1606(1-3):1-21.
[12] Anastacio MM,Kanter EM,Makepeace CM,et al. Relationship between mitochondrial matrix volume and cellular volume in response to stress and the role of ATP-sensitive potassium channel[J]. Circulation,2013,128(11 Suppl 1):S130-S135.
[13] Alberici LC,Oliveira HC,Paim BA,et al. Mitochondrial ATP-sensitive K(+) channels as redox signals to liver mitochondria in response to hypertriglyceridemia[J]. Free Radic Biol Med,2009,47(10):1432-1439.
[14] Jin C,Wu J,Watanabe M,et al. Mitochondrial K+ channels are involved in ischemic postconditioning in rat hearts[J]. J Physiol Sci,2012,62(4):325-332.
[15] Ziaeian B,Fonarow GC. Epidemiology and aetiology of heart failure[J]. Nature Reviews Cardiology,2016,13(6):368-378.
[16] Zhou HY,Zhang LN,Zheng MZ,et al. Improved myocardial function with supplement of levosimendan to Celsior solution[J]. J Cardiovasc Pharmacol,2014,64(3):256-265.
[17] Niwano S,Hirasawa S,Niwano H,et al. Cardioprotective effects of sarcolemmal and mitochondrial K-ATP channel openers in an experimental model of autoimmune myocarditis. Role of the reduction in calcium overload during acute heart failure[J]. Int Heart J,2012,53(2):139-145.
[18] Wang S,Guo X,Long CL,et al. SUR2B/Kir6.1 channel openers correct endothelial dysfunction in chronic heart failure via the miR-1-3p/ET-1 pathway[J]. Biomed Pharmacother,2019,110:431-439.
[19] Duan P,Wang J,Li Y,et al. Opening of mitoKATP improves cardiac function and inhibits apoptosis via the AKT-Foxo1 signaling pathway in diabetic cardiomyopathy[J]. Int J Mol Med,2018,42(5):2709-2719.
[20] Wang J,Bai J,Duan P,et al. Kir6.1 improves cardiac dysfunction in diabetic cardiomyopathy via the AKT-FoxO1 signalling pathway[J]. J Cell Mol Med,2021,25(8):3935-3949.
[21] Lemasters JJ. Selective mitochondrial autophagy,or mitophagy,as a targeted defense against oxidative stress,mitochondrial dysfunction,and aging[J]. Rejuvenation Res,2005,8(1):3-5.
[22] Nah J,Miyamoto S,Sadoshima J. Mitophagy as a protective mechanism against myocardial stress[J]. Compr Physiol,2017,7(4):1407-1424.
[23] Tan S,Wong E. Mitophagy Transcriptome:mechanistic insights into polyphenol-mediated mitophagy[J]. Oxid Med Cell Longev,2017,2017:9028435.
[24] Khaminets A,Behl C,Dikic I. Ubiquitin-dependent and independent signals in selective autophagy[J]. Trends Cell Biol,2016,26(1):6-16.
[25] Palikaras K,Lionaki E,Tavernarakis N. Mechanisms of mitophagy in cellular homeostasis,physiology and pathology[J]. Nat Cell Biol,2018,20(9):1013-1022.
[26] Villa E,Pro?cs E,Rubio-Pati?o C,et al. Parkin-independent mitophagy controls chemotherapeutic response in cancer cells[J]. Cell Rep,2017,20(12):2846-2859.
[27] Szargel R,Shani V,Abd Elghani F,et al. The PINK1,synphilin-1 and SIAH-1 complex constitutes a novel mitophagy pathway[J]. Hum Mol Genet,2016,25(16):3476-3490.
[28] Lazarou M,Sliter DA,Kane LA,et al. The ubiquitin kinase PINK1 recruits autophagy receptors to induce mitophagy[J]. Nature,2015,524(7565):309-314.
[29] Bakula D,Scheibye-Knudsen M. Mitophaging:mitophagy in aging and disease[J]. Front Cell Dev Biol,2020,8:239.
[30] Zhu Y,Massen S,Terenzio M,et al. Modulation of serines 17 and 24 in the LC3-interacting region of Bnip3 determines pro-survival mitophagy versus apoptosis[J]. J Biol Chem,2013,288(2):1099-1113.
[31] Rogov VV,Suzuki H,Marinkovi? M,et al. Phosphorylation of the mitochondrial autophagy receptor Nix enhances its interaction with LC3 proteins[J]. Sci Rep,2017,7(1):1131.
[32] Kuang Y,Ma K,Zhou C,et al. Structural basis for the phosphorylation of FUNDC1 LIR as a molecular switch of mitophagy[J]. Autophagy,2016,12(12):2363-2373.
[33] Chen G,Han Z,Feng D,et al. A regulatory signaling loop comprising the PGAM5 phosphatase and CK2 controls receptor-mediated mitophagy[J]. Mol Cell,2014,54(3):362-377.
[34] Chen M,Chen Z,Wang Y,et al. Mitophagy receptor FUNDC1 regulates mitochondrial dynamics and mitophagy[J]. Autophagy,2016,12(4):689-702.
[35] Qiu Z,Wei Y,Song Q,et al. The role of myocardial mitochondrial quality control in heart failure[J]. Front Pharmacol,2019,10:1404.
[36] Wang B,Nie J,Wu L,et al. AMPKα2 protects against the development of heart failure by enhancing mitophagy via PINK1 phosphorylation[J]. Circ Res,2018,122(5):712-729.
[37] Xiong W,Hua J,Liu Z,et al. PTEN induced putative kinase 1 (PINK1) alleviates angiotensin II-induced cardiac injury by ameliorating mitochondrial dysfunction[J]. Int J Cardiol,2018,266:198-205.
[38] Billia F,Hauck L,Konecny F,et al. PTEN-inducible kinase 1 (PINK1)/Park6 is indispensable for normal heart function[J]. Proc Natl Acad Sci U S A,2011,108(23):9572-9577.
[39] Xu W,Barrientos T,Mao L,et al. Lethal cardiomyopathy in mice lacking transferrin receptor in the heart[J]. Cell Rep,2015,13(3):533-545.
[40] Yu Z,Chen R,Li M,et al. Mitochondrial calcium uniporter inhibition provides cardioprotection in pressure overload-induced heart failure through autophagy enhancement[J]. Int J Cardiol,2018,271:161-168.
[41] Thai PN,Daugherty DJ,Frederich BJ,et al. Cardiac-specific conditional knockout of the 18-kDa mitochondrial translocator protein protects from pressure overload induced heart failure[J]. Sci Rep,2018,8(1):16213.
[42] Liu R,Zhang HB,Yang J,et al. Curcumin alleviates isoproterenol-induced cardiac hypertrophy and fibrosis through inhibition of autophagy and activation of mTOR[J]. Eur Rev Med Pharmacol Sci,2018,22(21):7500-7508.
[43] Huang CY,Lee FL,Peng SF,et al. HSF1 phosphorylation by ERK/GSK3 suppresses RNF126 to sustain IGF-IIR expression for hypertension-induced cardiomyocyte hypertrophy[J]. J Cell Physiol,2018,233(2):979-989.
[44] Huang CY,Kuo WW,Ho TJ,et al. Rab9-dependent autophagy is required for the IGF-IIR triggering mitophagy to eliminate damaged mitochondria[J]. J Cell Physiol,2018,233(9):7080-7091.
[45] Huang CY,Lai CH,Kuo CH,et al. Inhibition of ERK-Drp1 signaling and mitochondria fragmentation alleviates IGF-ⅡR-induced mitochondria dysfunction during heart failure[J]. J Mol Cell Cardiol,2018,122:58-68.
[46] Morales PE,Arias-Durán C,?valos-Guajardo Y,et al. Emerging role of mitophagy in cardiovascular physiology and pathology[J]. Mol Aspects Med,2020,71:100822.
[47] Sciarretta S,Maejima Y,Zablocki D,et al. The role of autophagy in the heart[J]. Annu Rev Physiol,2018,80:1-26.
[48] Hu ZL,Sun T,Lu M,et al. Kir6.1/K-ATP channel on astrocytes protects against dopaminergic neurodegeneration in the MPTP mouse model of Parkinson’s disease via promoting mitophagy[J]. Brain Behav Immun,2019,81:509-522.
[49] Mortensen SA,Rosenfeldt F,Kumar A,et al. The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure:results from Q-SYMBIO:a randomized double-blind trial[J]. JACC Heart Fail,2014,2(6):641-649.
[50] Daubert MA,Yow E,Dunn G,et al. Novel mitochondria-targeting peptide in heart failure treatment:a randomized,placebo-controlled trial of elamipretide[J]. Circ Heart Fail,2017,10(12):e004389.

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更新日期/Last Update: 2023-03-23