The underlying mechanism of calcium toxicity-induced autophagic cell death and lysosomal degradation in early stage of cerebral ischemia.
Jirakhamon SengkingPasuk MahakkanukrauhPublished in: Anatomy & cell biology (2024)
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 (Ca 2+ ) 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 Ca 2+ 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 Ca 2+ and autophagic process in acute stage of ischemic stroke.
Keyphrases
- cerebral ischemia
- cell death
- early stage
- subarachnoid hemorrhage
- blood brain barrier
- brain injury
- cell cycle arrest
- reactive oxygen species
- oxidative stress
- multiple sclerosis
- drug induced
- stem cells
- protein kinase
- liver failure
- cardiovascular events
- signaling pathway
- type diabetes
- cardiovascular disease
- body mass index
- lymph node
- ischemia reperfusion injury
- resting state
- endoplasmic reticulum stress
- cell therapy
- mesenchymal stem cells
- radiation therapy
- weight gain
- respiratory failure
- functional connectivity
- bone marrow
- physical activity
- aortic dissection
- neoadjuvant chemotherapy
- meta analyses