Anat Cell Biol 2024; 57(2): 155-162
Published online June 30, 2024
https://doi.org/10.5115/acb.24.003
Copyright © Korean Association of ANATOMISTS.
Jirakhamon Sengking1 , Pasuk Mahakkanukrauh1,2
1Department of Anatomy, Faculty of Medicine, Chiang Mai University, Chiang Mai, 2Excellence in Osteology Research and Training Center (ORTC), Chaing Mai University, Chiang Mai, Thailand
Correspondence to:Pasuk Mahakkanukrauh
Department of Anatomy & Excellence in Osteology Research and Training Center (ORTC), Chaing Mai University, Chiang Mai 50200, Thailand
E-mail: pasuk034@gmail.com
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Cerebral ischemia is the important cause of worldwide disability and mortality, that is one of the obstruction of blood vessels supplying to the brain. In early stage, glutamate excitotoxicity and high level of intracellular calcium (Ca2+) are the major processes which can promote many downstream signaling involving in neuronal death and brain tissue damaging. Moreover, autophagy, the reusing of damaged cell organelles, is affected in early ischemia. Under ischemic conditions, autophagy plays an important role to maintain energy of the brain and its function. In the other hand, over intracellular Ca2+ accumulation triggers excessive autophagic process and lysosomal degradation leading to autophagic process impairment which finally induce neuronal death. This article reviews the association between intracellular Ca2+ and autophagic process in acute stage of ischemic stroke.
Keywords: Cerebral ischemia, Calcium toxicity, Autophagy, Lysosomal degradation, Neuronal cell death