Neural Regeneration Research ›› 2018, Vol. 13 ›› Issue (3): 556-562.doi: 10.4103/1673-5374.228762

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Regulatory role of calpain in neuronal death

Si-ying Cheng1, Shu-chao Wang2, Ming Lei1, Zhen Wang2, Kun Xiong2   

  1. 1 Xiangya Medical School, Central South University, Changsha, Hunan Province, China
    2 Department of Anatomy and Neurobiology, School of Basic Medical Sciences, Central South University, Changsha, Hunan Province, China
  • Received:2017-12-26 Online:2018-03-15 Published:2018-03-15
  • Contact: Kun Xiong, Ph.D.,xiongkun2001@163.com.
  • Supported by:

    This study was supported by the National Natural Science Foundation of China, No. 81571939 & 81772134; the Wu Jie-Ping Medical Foundation of the Minister of Health of China, No. 320.6750.14118; the Natural Science Foundation of Hunan Province of China, No.2015JJ2187; the Teacher Research Foundation of Central South University of China, No. 2014JSJJ026.

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Abstract:

Calpains are a group of calcium-dependent proteases that are over activated by increased intracellular calcium levels under pathological conditions. A wide range of substrates that regulate necrotic, apoptotic and autophagic pathways are affected by calpain. Calpain plays a very important role in neuronal death and various neurological disorders. This review introduces recent research progress related to the regulatory mechanisms of calpain in neuronal death. Various neuronal programmed death pathways including apoptosis, autophagy and regulated necrosis can be divided into receptor interacting protein-dependent necroptosis, mitochondrial permeability transition-dependent necrosis, pyroptosis and poly (ADP-ribose)polymerase 1-mediated parthanatos. Calpains cleave series of key substrates that may lead to cell death or participate in cell death. Regarding the investigation of calpain-mediated programed cell death, it is necessary to identify specific inhibitors that inhibit calpain mediated neuronal death and nervous system diseases.

Key words: nerve regeneration, calpain, calpastatin, central nervous system, apoptosis, autophagy, B-cell lymphoma, cyclin-dependent kinases, mitochondrial permeability transition, neural regeneration