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Related Experiment Video

Updated: Jun 17, 2026

Implantation of Miniosmotic Pumps and Delivery of Tract Tracers to Study Brain Reorganization in Pathophysiological Conditions

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Published on: January 18, 2016

ATF5-Dependent GDF15 Expression Mediates Anesthesia-Induced Neuroprotection Against Stroke.

Xianshu Ju^1,2,3, Tao Zhang^1,2,3, Jianchen Cui⁴

¹Department of Medical Science, Chungnam National University School of Medicine, Daejeon, 35015, South Korea.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)

|November 26, 2025

Summary

Sevoflurane anesthesia may protect the brain against stroke by activating mitochondrial stress responses. However, this protective effect is lost in aged brains, necessitating age-specific stroke prevention strategies.

Keywords:

ATF5 / GDF15 anesthesia preconditioning stroke

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Area of Science:

Neuroscience
Anesthesiology
Mitochondrial Biology

Background:

Perioperative stroke is a serious complication, particularly in aging populations.
Anesthetics like sevoflurane show preclinical neuroprotection against ischemic injury, but clinical evidence is inconclusive.
Aging may impair the brain's ability to respond to stress.

Purpose of the Study:

To investigate the molecular mechanisms of sevoflurane-induced neuroprotection.
To determine the role of mitochondrial pathways in sevoflurane's effects.
To assess whether aging affects sevoflurane's neuroprotective capacity.

Main Methods:

Gene expression analysis in cerebral cortex.
Focus on mitochondrial unfolded protein response (UPRmt) and bioenergetic metabolism.
Investigation of ATF5 (activating transcription factor-5) and GDF15 expression.

Main Results:

Sevoflurane upregulates UPRmt and mitochondrial metabolism genes, including ATF5 and GDF15.
ATF5 plays a crucial role in mediating sevoflurane's protective effects.
This protective mechanism is absent in the aged brain.

Conclusions:

Sevoflurane-induced neuroprotection relies on activating mitochondrial stress responses via ATF5.
Aging diminishes the brain's capacity to activate these protective mitochondrial pathways.
Age-specific strategies targeting mitochondrial function are needed to mitigate perioperative stroke risk in elderly patients.