TRPC6-Mediated Ca2+ Signaling is Required for Hypoxia-Induced Autophagy in Human Podocytes
Author(s) -
Tianrong Ji,
Chengwei Zhang,
Linlin Ma,
Qin Wang,
Li Zou,
Kexin Meng,
Rui Zhang,
Jundong Jiao
Publication year - 2018
Publication title -
cellular physiology and biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.486
H-Index - 87
eISSN - 1421-9778
pISSN - 1015-8987
DOI - 10.1159/000492351
Subject(s) - trpc6 , autophagy , microbiology and biotechnology , hypoxia (environmental) , intracellular , signal transduction , ampk , chemistry , activator (genetics) , biology , protein kinase a , kinase , transient receptor potential channel , receptor , biochemistry , apoptosis , organic chemistry , oxygen
Intracellular Ca2+ signaling plays an important role in the regulation of autophagy. However, very little is known about the role of Ca2+ influx, which is induced by plasma membrane Ca2+ channels. Our previous study showed that transient receptor potential canonical channel-6 (TRPC6), a major Ca2+ influx pathway in podocytes, was activated by hypoxia. Here, we investigated whether TRPC6 is involved in hypoxia-induced autophagy in cultured human podocytes.
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