心肌细胞钙稳态失调在心力衰竭中作用的研究进展

doi:10.16352/j.issn.1001-6325.2022.03.008

基础医学与临床 ›› 2022, Vol. 42 ›› Issue (3): 502-506.doi: 10.16352/j.issn.1001-6325.2022.03.008

心肌细胞钙稳态失调在心力衰竭中作用的研究进展

刘峰宇, 韩薇^*

哈尔滨医科大学附属第一医院心血管内科, 黑龙江哈尔滨 150000

收稿日期:2020-10-09 修回日期:2021-01-09 出版日期:2022-03-05 发布日期:2022-03-04
通讯作者: ^* dr.hanwei@foxmail.com
基金资助:
黑龙江省自然科学基金(ZD2020H002); 上海市浦东新区卫生系统重点学科项目(PWZxk2017-01)

Research progress on the role of myocardial cell calcium homeostasis dysregulation in heart failure

LIU Feng-yu, HAN Wei^*

Department of Cardiology,the First Affliated Hospital of Harbin Medical University,Harbin 150000,China

Received:2020-10-09 Revised:2021-01-09 Online:2022-03-05 Published:2022-03-04
Contact: ^* dr.hanwei@foxmail.com

摘要/Abstract

摘要： 心肌细胞的钙稳态依赖于质膜、肌/内质网(SR)、线粒体等对钙(Ca²⁺)转运的调节。胞质钙超载、SR钙渗漏等在内的钙稳态失调,使心肌细胞钙瞬变减低,收缩力下降是心力衰竭的主要特征之一。

关键词: 钙稳态, 心力衰竭, 钙ATP酶2a, 2型兰尼碱受体(RyR2)

Abstract: Calcium homeostasis of cardiomyocytes depends on the regulation of calcium(Ca²⁺) transportation through plasma membrane, sarco/endoplasmic reticulum(SR) and mitochondria. One of the main characteristics of heart failure is calcium homeostasis, including cytosolic calcium overload and SR calcium leakage, which leads to transient decrease of myocardial calcium and decrease of contractility.

Key words: calcium homeostasis, heart failure, calcium ATPase 2a, ryanodine receptor 2(RyR2)

中图分类号:

R541

刘峰宇, 韩薇. 心肌细胞钙稳态失调在心力衰竭中作用的研究进展[J]. 基础医学与临床, 2022, 42(3): 502-506.

LIU Feng-yu, HAN Wei. Research progress on the role of myocardial cell calcium homeostasis dysregulation in heart failure[J]. Basic & Clinical Medicine, 2022, 42(3): 502-506.

参考文献

[1]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, 2018,46:760-789.
[2]Fink BD, Bai F, Yu L, et al. Regulation of ATP production: dependence on calcium concentration and respiratory state[J]. Am J Physiol Cell Physiol, 2017,313:C146-C153.
[3]Landstrom AP, Dobrev D, Wehrens X. Calcium signaling and cardiac arrhythmias[J]. Circ Res, 2017,120:1969-1993.
[4]Sanchez-Alonso JL, Loucks A, Schobesberger S, et al. Nanoscale regulation of L-type calcium channels differentiates between ischemic and dilated cardiomyopathies[J]. E Bio Med, 2020,57:102845.doi:10.1016/j.ebiom.2020.102845.
[5]Gross P, Johnson J, Romero CM, et al. Interaction of the joining region in junctophilin-2 with the L-type Ca²⁺ channel is pivotal for cardiac dyad assembly and intracellular Ca²⁺ dynamics[J]. Circ Res, 2020.doi:10.1161/CIRCRESAHA.119.315715
[6]Wang X, Zhuo X, Gao J, et al. Neuregulin-1β partially improves cardiac function in volume-overload heart failure through regulation of abnormal calcium handling[J]. Front Pharmacol, 2019,10:616.doi:10.3389/fphar.2019.00616.
[7]Primessnig U, Bracic T, Levijoki J, et al. Long-term effects of Na⁺/Ca²⁺ exchanger inhibition with ORM-11035 improves cardiac function and remodelling without lowering blood pressure in a model of heart failure with preserved ejection fraction[J]. Eur J Heart Fail, 2019,21:1543-1552.
[8]Eder P. Cardiac remodeling and disease: SOCE and TRPC signaling in cardiac pathology[J]. Adv Exp Med Biol, 2017,993:505-521.
[9]Bartoli F, Bailey MA, Rode B, et al. Orai1 channel inhibition preserves left ventricular systolic function and normal Ca²⁺ handling after pressure overload[J]. Circulation, 2020,141:199-216.
[10]Kho C, Lee A, Jeong D, et al. Small-molecule activation of SERCA2a SUMOylation for the treatment of heart failure[J]. Nat Commun, 2015,6:7229.
[11]Kolstad TR, van den Brink J, MacQuaide N, et al. Ryanodine receptor dispersion disrupts Ca²⁺ release in failing cardiac myocytes[J]. eLife, 2018,7.doi:10.7554/eLife.39427
[12]Zhang Y, Wang WE, Zhang X, et al. Cardiomyocyte PKA ablation enhances basal contractility while eliminates cardiac β-adrenergic response without adverse effects on the heart[J]. Circ Res, 2019,124:1760-1777.
[13]Pollak AJ, Liu C, Gudlur A, et al. A secretory pathway kinase regulates sarcoplasmic reticulum Ca²⁺ homeostasis and protects against heart failure[J]. eLife, 2018,7.doi:10.7554/eLife.41378
[14]Pollak AJ, Haghighi K, Kunduri S, et al. Phosphoryla-tion of serine96 of histidine-rich calcium-binding protein by the Fam20C kinase functions to prevent cardiac arrhythmia[J]. Proc Nati Acad Sci U S A, 2017,114:9098-9103.
[15]Kwong JQ. The mitochondrial calcium uniporter in the heart: energetics and beyond[J]. J Physiol, 2017,595:3743-3751.
[16]Zaglia T, Ceriotti P, Campo A, et al. Content of mitochondrial calcium uniporter (MCU) in cardiomyocytes is regulated by microRNA-1 in physiologic and pathologic hypertrophy[J]. Proc Natl Acad Sci USA, 2017,114:E9006-E9015.
[17]Yu Z, Chen R, Li M, et al. Mitochondrial calcium uniporter inhibition provides cardioprotection in pressure overload-induced heart failure through autophagy enhancement[J].Inter J Cardiol, 2018,271:161-168.
[18]吴锦波, 叶小汉, 冼绍祥, 等. 比索洛尔提高心力衰竭大鼠心肌SERCA2a活性[J]. 基础医学与临床,2017, 37: 386-390.
[19]Hulot JS, Salem JE, Redheuil A, et al. Effect of intracoronary administration of AAV1/SERCA2a on ventricular remodelling in patients with advanced systolic heart failure: results from the AGENT-HF randomized phase 2 trial[J]. Eur J Heart Fail, 2017,19:1534-1541.
[20]Lyon AR, Babalis D, Morley-Smith AC, et al. Investiga-tion of the safety and feasibility of AAV1/SERCA2a gene transfer in patients with chronic heart failure supported with a left ventricular assist device-the SERCA-LVAD TRIAL[J]. Gene Ther, 2020,27:579-590.
[21]Gorski PA, Jang SP, Jeong D, et al. Role of SIRT1 in modulating acetylation of the sarco-endoplasmic reticulum Ca²⁺-ATPase in heart failure[J]. Circulation Res, 2019,124:e63-e80.
[22]Keceli G, Majumdar A, Thorpe CN, et al. Nitroxyl (HNO) targets phospholamban cysteines 41 and 46 to enhance cardiac function[J]. J Gen Physiol, 2019,151:758-770.
[23]Felker GM, Borentain M, Cleland JG, et al. Rationale and design for the development of a novel nitroxyl donor in patients with acute heart failure[J]. Eur J Heart Fail, 2019,21:1022-1031.
[24]Kobayashi S, Wakeyama T, Ono S, et al. A multicenter, randomized, double-blind, controlled study to evaluate the efficacy and safety of dantrolene on ventricular arrhythmia as well as mortality and morbidity in patients with chronic heart failure (SHO-IN trial): rationale and design[J]. J Cardiol, 2020,75:454-461.
[25]Ashna A, van Helden DF, Dos Remedios C, et al. Phenytoin reduces activity of cardiac ryanodine receptor 2; a potential mechanism for its cardioprotective action[J]. Mol Pharmacol, 2020,97:250-258.

心肌细胞钙稳态失调在心力衰竭中作用的研究进展

Research progress on the role of myocardial cell calcium homeostasis dysregulation in heart failure

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 12

编辑推荐

Metrics

本文评价

[1]	王放董哲孙艺红任景怡李菁周益锋郑金刚. 影响非缺血性心力衰竭患者心肌纤维化的因素分析[J]. 基础医学与临床, 2021, 41(3): 346-351.
[2]	张志敏苟丽沙马丽群任可路军魏星李慧杰周圣华. 达格列净降低心力衰竭大鼠心肌内质网应激并缓解左室重构[J]. 基础医学与临床, 2021, 41(12): 1742-1748.
[3]	刘颖娴宋彦君陈未林雪赖晋智黎婧怡吴炜. 非缺血性心力衰竭患者应用伊伐布雷定的有效性与安全性评价[J]. 基础医学与临床, 2021, 41(11): 1637-1642.
[4]	吕芳徐晓杰高鹏宋玉文夏维波邢小平李梅. TMEM38B纯合突变导致罕见XIV型成骨不全症[J]. 基础医学与临床, 2018, 38(5): 594-599.
[5]	胡欢李萍程晓曙. 线粒体融合-分裂与心力衰竭[J]. 基础医学与临床, 2018, 38(4): 553-556.
[6]	徐建平杨保卫. Ghrelin对心衰恶液质的治疗作用*[J]. 基础医学与临床, 2012, 32(1): 102-105.
[7]	李英莲李维善. 青海地区老年人心力衰竭患者血浆BNP水平变化与临床观察分析[J]. 基础医学与临床, 2010, 30(2): 205-205.
[8]	杨华沈珠军. 脂肪来源细胞在缺血性心脏病中的应用[J]. 基础医学与临床, 2010, 30(11): 1226-1229.
[9]	孔一慧曹荣元张莉刘玉冰李悦李为民. β3肾上腺素能受体激动剂和抑制剂对心衰大鼠心室MMP2和9表达的影响[J]. 基础医学与临床, 2010, 30(11): 1177-1183.
[10]	刘洪岩张金国谭洪勇. 慢性心力衰竭患者血浆APN水平与BNP、TNF-α、IR相关性[J]. 基础医学与临床, 2010, 30(10): 1098-1099.
[11]	王蕾王海鹏赵彩明韩莲花邹操刘志华蒋文平. 兔舒张性心衰和收缩性心衰模型建立及间质重构的比较[J]. 基础医学与临床, 2009, 29(12): 1244-1248.
[12]	邱红朱红枫. 氯沙坦降低心力衰竭大鼠心肌细胞凋亡[J]. 基础医学与临床, 2009, 29(11): 1207-1210.