Hyperglycaemia Stress-Induced Renal Injury is Caused by Extensive Mitochondrial Fragmentation, Attenuated MKP1 Signalling, and Activated JNK-CaMKII-Fis1 Biological Axis | Zendy

Yunfang Zhang | Zendy; Junxia Feng | Zendy; Qi Wang | Zendy; Shili Zhao | Zendy; Shen Yang | Zendy; Lü Tian | Zendy; Ping Meng | Zendy; Jingchun Li | Zendy; Hongyan Li | Zendy

Open Access

Hyperglycaemia Stress-Induced Renal Injury is Caused by Extensive Mitochondrial Fragmentation, Attenuated MKP1 Signalling, and Activated JNK-CaMKII-Fis1 Biological Axis

Author(s) -

Yunfang Zhang,

Junxia Feng,

Qi Wang,

Shili Zhao,

Shen Yang,

Lü Tian,

Ping Meng,

Jingchun Li,

Hongyan Li

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 - 10.1159/000495681

Subject(s) - mitochondrial permeability transition pore , biology , microbiology and biotechnology , mitochondrion , apoptosis , oxidative stress , endocrinology , cancer research , programmed cell death , biochemistry

Hyperglycaemia stress-induced renal injury is closely associated with mitochondrial dysfunction through poorly understood mechanisms. The aim of our study is to explore the upstream trigger and the downstream effector driving diabetic nephropathy via modulating mitochondrial homeostasis.

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