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This document summarizes a research paper that investigates how heat shock protein 22 (hsp22) modulates mitochondrial function to alleviate early brain injury from subarachnoid hemorrhage in rats. The study found that hsp22 treatment maintained neurological function, reduced brain edema, and improved oxidative stress and mitochondrial apoptosis by salvaging mitochondrial homeostasis in an AMPK-PGC1α dependent manner. This modulated mitochondrial biogenesis and fission, reducing oxidative stress and brain in

Author

Kurtis

Language

EN