Calcium ion--the key player in cerebral ischemia

• Published in: Current medicinal chemistry Vol. 21; no. 18; p. 2065
• Main Authors: Kumar, V S Suvanish, Gopalakrishnan, A, Naziroğlu, M, Rajanikant, G K
• Format: Journal Article
• Language: English
• Published: United Arab Emirates 2014
• Subjects: Animals; Brain Ischemia - metabolism; Brain Ischemia - pathology; Calcium - metabolism; Calcium Channels - metabolism; Cell Death; Homeostasis; Humans; Neurons - metabolism
• ISSN: 1875-533X
• DOI: 10.2174/0929867321666131228204246

Role of calcium ion (Ca2+) in the functioning of neurons from their naïve state to mature state is of vital importance. It controls functions such as neuronal functioning, neuronal ATP production, central nervous system migration and many others. Failure in Ca2+ homeostasis mechanisms and the resulting cellular Ca2+ ion load initiates a cascade of reactions involving various cytosolic enzymes and proteins. This total mechanism leads to the neuronal death. The ability of neurons to resist such death mechanisms fails as a result of extensive cell death signaling cascade reactions and later brings brain damage. The role of neuronal endoplasmic reticulum and protein channels like CaVs, TRP channels, and NMDAR as the mediators of cell damage and death has been evaluated in the studies related to cerebral ischemia. Here, we portray Ca2+ ion as one of the role players in neuronal death and cerebral damage following ischemia. The role of Ca2+ in neuronal functioning, its regulatory mechanisms and the failure of homeostatic mechanisms are discussed in detail.