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
- drug induced
- oxidative stress
- protein kinase
- multiple sclerosis
- sentinel lymph node
- randomized controlled trial
- systematic review
- cardiovascular events
- atrial fibrillation
- stem cells
- high glucose
- cell therapy
- body mass index
- signaling pathway
- intensive care unit
- diabetic rats
- risk factors
- weight gain
- radiation therapy
- neoadjuvant chemotherapy
- endoplasmic reticulum stress
- aortic dissection
- rectal cancer
- mesenchymal stem cells
- meta analyses