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Mitochondrial dysfunction - Silent killer in cerebral ischemia.

Abstract：

:Mitochondrial dysfunction aggravates ischemic neuronal injury through activation of various pathophysiological and molecular mechanisms. Ischemic neuronal injury is particularly intensified during reperfusion due to impairment of mitochondrial function. Mitochondrial mutilation instigates alterations in calcium homeostasis in neurons, which plays a pivotal role in the maintenance of normal neuronal function. Increase in intracellular calcium level in mitochondria triggers the opening of mitochondrial transition pore and over production of reactive oxygen species (ROS). Several investigations have concluded that ROS not only contribute to lipids and proteins damage, but also transduce apoptotic signals leading to neuronal death. In addition to the above mentioned reasons, endoplasmic reticulum (ER) stress due to excitotoxicity also leads to neuronal death. Recently, some newer proteins have been claimed to induce "mitophagy" by triggering the receptors on autophagic membranes leading to neurodegeneration. This review summarizes the mechanisms underlying neuronal death involving mitochondrial dysfunction and mitophagy.

journal_name

J Neurol Sci

journal_title

Journal of the neurological sciences

authors

Bakthavachalam P,Shanmugam PST

doi

10.1016/j.jns.2017.02.043

subject

Has Abstract

pub_date

2017-04-15 00:00:00

pages

417-423

eissn

0022-510X

issn

1878-5883

pii

S0022-510X(17)30139-9

journal_volume

375

pub_type

杂志文章,评审

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