肌浆网/内质网钙调控在心血管疾病中的研究进展
《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]
- 期数:
- 2015年第2期
- 页码:
- 216-220
- 栏目:
- 综述
- 出版日期:
- 2014-10-25
文章信息/Info
- Title:
- Recent progress of sarcoplasmic/endoplasmic reticulum calcium regulation in cardiovascular diseases
- Author(s):
- XU Man; LU Xing-zhu; BI Xue-yuan; ZHAO Ming; ZANG Wei-jin
- (Department of Pharmacology, Health Science Center, Xi’an Jiaotong University, Xi’an 710061, Shaanxi, China)
- 分类号:
- R54
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 肌浆网/内质网（SR/ER）是细胞内重要的钙储库及调控系统，主要通过Ca2+释放通道雷尼丁受体（RyR）和1,4,5-三磷酸肌醇受体（IP3R），以及Ca2+摄取蛋白肌浆网Ca2+-ATP酶（SERCA）和基质交感分子1（STIM1）等调节钙信号，维持细胞内钙稳态。研究发现，SR/ER钙平衡对细胞正常生理功能的发挥和信息传递非常重要，SR/ER钙稳态失调与缺血性心脏病、心肌肥厚、高血压及心力衰竭等心血管疾病的发生发展密切相关。本文就SR/ER钙调控在心血管疾病中的研究进展作一概述，重点阐述SR/ER钙离子通道和相关调控蛋白对细胞内钙信号的调节机制，以期为临床心血管疾病的治疗提供重要策略和潜在靶点。
- Abstract:
- Sarcoplasmic/endoplasmic reticulum (SR/ER), an intracelluar Ca2+ store, plays a pivotal role in regulating Ca2+ signals. Ca2+ homeostasis is exquisitely controlled by regulatory proteins in SR/ER, including ryanodine receptor (RyR), inositol 1,4,5-trisphosphate receptor (IP3R), sarcoplasmic reticulum Ca2+ ATPase (SERCA) and stromal interaction molecule1 (STIM1). Recent studies have shown that maintaining Ca2+ homeostasis is of great importance in maintaining normal cell physiological functions and signal transduction. Alterations in Ca2+ homeostasis are essential in the occurrence and development of various cardiovascular diseases such as ischemic heart disease, myocardial hypertrophy, hypertension and heart failure. This review is focused on the recent progress of SR/ER Ca2+ regulation in cardiovascular diseases, particularly the modulatory mechanisms of Ca2+ channels and related Ca2+ handling protein. Research on SR/ER Ca2+ regulation will provide promising strategies and potential targets for therapy of cardiovascular diseases.
参考文献/References
[1]Fischer TH,Maier LS,Sossalla S.The ryanodine receptor leak:how a tattered receptor plunges the failing heart into crisis[J].Heart Fail Rev,2013,18(4):475-483.
[2]Kaloqeris T,Baines CP,Krenz M,et al.Cell biology of ischemia/reperfusion injury[J].Int Rev Cell Mol Biol,2012,298:229-317.
[3]张 林,王蓓蕾,肖 良,等.RyR2/Ca~(2+)释放通道在心脏生理与疾病中的作用[J].心脏杂志,2012,24(4):525-528.
[4]Subramanian M,Jayakumar S,Richhariya S,et al.Loss of IP3 receptor function in neuropeptide secreting neurons leads to obesity in adult Drosophila[J].BMC Neurosci,2013,14:157.
[5]Monaco G,Decrock E,Nuyts K,et al.Alpha-helical destabilization of the Bcl-2-BH4-domain peptide abolishes its ability to inhibit the IP3 receptor[J].PLoS One,2013,8(8):e73386.
[6]Kranias EG,Hajjar RJ.Modulation of cardiac contractility by the phospholamban/SERCA2a regulatome[J].Circ Res,2012,110(12):1646-1660.
[7]贺 熙,毕学苑,王 皓,等.心血管缺血再灌注损伤钙调控的研究进展[J].生理学报,2012,64(3):321-326.
[8]Pani B,Bolimuntha S,Singh BB.The TR (i)P to Ca2+signaling just got STIMy:an update on STIM1 activated TRPC channels[J].Front Biosci(Landmark Ed),2012,17:805-823.
[9]Peglow M,Niemeyer BA,Hoth M,et al.Interplay of channels, pumps and organelle location in Calcium microdomain formation[J].New J Phys,2013,15(5):055022.
[10]Gerasimenko JV,Gryshchenko O,Ferdek PE,et al.Ca2+release-activated Ca2+ Channel blockade as a potential tool in antipancreatitis therapy[J].Proc Natl Acad Sci U S A,2013,110(32):13186-13191.
[11]Zhang X,Yan SM,Zheng HL,et al.A mechanism underlying hypertensive occurrence in the metabolic syndrome:cooperative effect of oxidative stress and Calcium accumulation in vascular smooth muscle cells[J].Horm Metab Res,2014,46(2):126-132.
[12]Ding F,Qian B,Zhao X,et al.VPPIPP and IPPVPP: two hexapeptides innovated to exert antihypertensive activity[J].PLoS One,2013,8(4):e62384.
[13]Abou-Saleh H,Pathan AR,Daalis A,et al.Inositol 1,4,5-trisphosphate(IP3)receptor up-regulation in hypertension is associated with sensitization of Ca2+ release and vascular smooth muscle contractility[J].J Biol Chem,2013,288(46):32941-32951.
[14]Giachini FR,Lima VV,Filgueira FP,et al.STIM1/Orai1 contributes to sex differences in vascular responses to Calcium in spontaneously hypertensive rats[J].Clin Sci,2012,122(5):215-226.
[15]Luo X,Hojayev B,Jiang N,et al.STIM1-dependent store-operated Ca?? entry is required for pathological cardiac hypertrophy[J].J Mol Cell Cardiol,2012,52(1):136-147.
[16]Xing Y,Gao Y,Chen J,et al.Wenxin-Keli regulates the Calcium/Calmodulin-Dependent protein kinase II signal transduction pathway and inhibits cardiac arrhythmia in rats with myocardial infarction[J].Evid Based Complement Alternat Med,2013,2013:464508.
[17]Okada H,Lai NC,Kawaraguchi Y,et al.Integrins protect cardiomyocytes from ischemia/reperfusion injury[J].J Clin Invest,2013,123(10):4294-4308.
[18]Li Y,Zhu W,Tao J,et al.Fasudil protects the heart against ischemia-reperfusion injury by attenuating endoplasmic reticulum stress and modulating SERCA activity:the differential role for PI3K/Akt and JAK2/STAT3 signaling pathways[J].PLoS One,2012,7(10):e48115.
[19]Zima AV,Bovo E,Mazurek SR,et al.Cahandling during excitation-contraction coupling in heart failure[J].Pflugers Arch,2014,466(6):1129-1137.
[20]Respress JL,van Oort RJ,Li N,et al.Role of RyR2 phosphorylation at S2814 during heart failure progression[J].Circ Res, 2012, 110(11):1474-1483.
[21]Hino A,Yano M,Kato T,et al.Enhanced binding of calmodulin to the ryanodine receptor corrects contractile dysfunction in failing hearts[J].Cardiovasc Res,2012,96(3):433-443.
备注/Memo
- 备注/Memo:
- 收稿日期：2014-04-18.
基金项目：国家自然科学基金重大国际(地区)合作项目资助（81120108002）；高等学校博士学科点专项科研基金优先发展领域课题资助（20130201130008）；陕西省自然科学基金项目资助（2012JZ4001）;中华医学基金会杰出教授奖资助（F510000/G16916404）
通讯作者：臧伟进，教授，主要从事心血管生理药理学研究上所述Email：zwj@mail.xjtu.edu.cn
作者简介：徐曼，硕士生 Email：xuman19
常用功能
统计/Statistics
- 摘要浏览/Viewed758
- 评论/Comments
