T-type voltage-gated channels, Na+/Ca2+-exchanger, and calpain-2 promote photoreceptor cell death in inherited retinal degeneration

被引:0
作者
Jie Yan
Lan Wang
Qian-Lu Yang
Qian-Xi Yang
Xinyi He
Yujie Dong
Zhulin Hu
Mathias W. Seeliger
Kangwei Jiao
François Paquet-Durand
机构
[1] Affiliated Hospital of Yunnan University,Yunnan Eye Institute & Key Laboratory of Yunnan Province, Yunnan Eye Disease Clinical Medical Center
[2] Yunnan University,Cell Death Mechanism Group, Institute for Ophthalmic Research
[3] University of Tübingen,Graduate Training Centre of Neuroscience
[4] University of Tübingen,High
[5] The Third Affiliated Hospital of Kunming Medical University &Yunnan Cancer Hospital,resolution Functional Imaging and Test Group, Institute for Ophthalmic Research
[6] University of Tübingen,Division of Ocular Neurodegeneration, Institute for Ophthalmic Research
[7] University of Tübingen,undefined
来源
Cell Communication and Signaling | / 22卷
关键词
Retinitis pigmentosa; Calcium channels; cGMP; HDAC; PAR; SOCE;
D O I
暂无
中图分类号
学科分类号
摘要
Inherited retinal degenerations (IRDs) are a group of untreatable and commonly blinding diseases characterized by progressive photoreceptor loss. IRD pathology has been linked to an excessive activation of cyclic nucleotide-gated channels (CNGC) leading to Na+- and Ca2+-influx, subsequent activation of voltage-gated Ca2+-channels (VGCC), and further Ca2+ influx. However, a connection between excessive Ca2+ influx and photoreceptor loss has yet to be proven.
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