Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2020 Feb 17;16(8):1303–1323. doi: 10.7150/ijbs.38962

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© The author(s)

This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/). See http://ivyspring.com/terms for full terms and conditions.

PMC Copyright notice

Schematic representation of the proposed anti-apoptotic signaling pathways triggered by ALDH2 in ischemic neurons. Cerebral ischemic reperfusion injury caused ALDH2 downregulation, leading to an increase in mitochondrial ROS (mROS) production. ROS served as a potential inducer of JNK. Then, activated JNK initiated the pro-apoptotic Cyt-C leakage from mitochondria into cytoplasm, launching the caspase-9 related mitochondrial apoptosis. Meanwhile, phosphorylated JNK was also bound to the caspase-3 promoter, leading to caspase-3 transcriptional activation. However, recovery of ALDH2 activity could cut off the excessive mROS and mitochondria-dependent apoptosis, providing prosurvival advantages for the brain in the context of ischemic injury.