Calcium Signaling Regulates Autophagy and Apoptosis.
Calcium Signaling Regulates Autophagy and Apoptosis.
复制标题
DOI:
10.3390/cells10082125
复制
发表时间:
2021-08-18
期刊:
影响因子:
6
通讯作者:
Singh BB
中科院分区:
文献类型:
--
作者:
Sukumaran P;Nascimento Da Conceicao V;Sun Y;Ahamad N;Saraiva LR;Selvaraj S;Singh BB
Calcium (Ca2+) functions as a second messenger that is critical in regulating fundamental physiological functions such as cell growth/development, cell survival, neuronal development and/or the maintenance of cellular functions. The coordination among various proteins/pumps/Ca2+ channels and Ca2+ storage in various organelles is critical in maintaining cytosolic Ca2+ levels that provide the spatial resolution needed for cellular homeostasis. An important regulatory aspect of Ca2+ homeostasis is a store operated Ca2+ entry (SOCE) mechanism that is activated by the depletion of Ca2+ from internal ER stores and has gained much attention for influencing functions in both excitable and non-excitable cells. Ca2+ has been shown to regulate opposing functions such as autophagy, that promote cell survival; on the other hand, Ca2+ also regulates programmed cell death processes such as apoptosis. The functional significance of the TRP/Orai channels has been elaborately studied; however, information on how they can modulate opposing functions and modulate function in excitable and non-excitable cells is limited. Importantly, perturbations in SOCE have been implicated in a spectrum of pathological neurodegenerative conditions. The critical role of autophagy machinery in the pathogenesis of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s diseases, would presumably unveil avenues for plausible therapeutic interventions for these diseases. We thus review the role of SOCE-regulated Ca2+ signaling in modulating these diverse functions in stem cell, immune regulation and neuromodulation.
登录
查看更多内容
影响因子:
5.8
作者:
Chauhan A;Sun Y;Sukumaran P;Quenum Zangbede FO;Jondle CN;Sharma A;Evans DL;Chauhan P;Szlabick RE;Aaland MO;Birnbaumer L;Sharma J;Singh BB;Mishra BB
通讯作者:
Mishra BB
影响因子:
4.1
作者:
Ahamad N;Singh BB
通讯作者:
Singh BB
影响因子:
64.5
作者:
Cárdenas C;Miller RA;Smith I;Bui T;Molgó J;Müller M;Vais H;Cheung KH;Yang J;Parker I;Thompson CB;Birnbaum MJ;Hallows KR;Foskett JK
通讯作者:
Foskett JK
影响因子:
5.3
作者:
Boland, Barry;Kumar, Asok;Lee, Sooyeon;Platt, Frances M.;Wegiel, Jerzy;Yu, W. Haung;Nixon, Ralph A.
通讯作者:
Nixon, Ralph A.
影响因子:
14.8
作者:
Barmada, Sami J.;Serio, Andrea;Arjun, Arpana;Bilican, Bilada;Daub, Aaron;Ando, D. Michael;Tsvetkov, Andrey;Pleiss, Michael;Li, Xingli;Peisach, Daniel;Shaw, Christopher;Chandran, Siddharthan;Finkbeiner, Steven
通讯作者:
Finkbeiner, Steven