Restoring cardiolipin homeostasis mitigates cerebral ischemia-reperfusion injury by suppressing ATG5-mediated neuronal autophagy-dependent ferroptosis
Quick Facts
- Publication title: Restoring cardiolipin homeostasis mitigates cerebral ischemia-reperfusion injury by suppressing ATG5-mediated neuronal autophagy-dependent ferroptosis
- Journal: J Adv Res
- Year: 2026
- DOI: 10.1016/j.jare.2026.03.014
- PMID/PMCID: 41831680
Research overview
This study aimed to characterize CL alterations following cerebral I/R injury, identify potential mechanisms underlying CL loss, and investigate the pathophysiological effects of these changes. However, their roles in cerebral ischemia/reperfusion (I/R) injury remains largely underexplored.
Key findings
Significant CL depletion and acyl chain remodeling were observed in peri-infarct brain tissues.
EV-mediated release was identified as one of the mechanisms of CL loss, and inhibiting EV release restored neuronal CL levels.
SS-31 inhibits CL release, preserves CL content, and subsequently restores CL homeostasis.
Restoring CL homeostasis attenuated cerebral I/R injury by suppressing neuronal ferroptosis.
Study design
Ischemic stroke was modeled by using middle cerebral occlusion/reperfusion (MCAO/R) in mice and oxygen-glucose deprivation/reoxygenation (OGD/R) in vitro.
CL alterations following cerebral I/R injury were evaluated through lipidomic analysis and fluorescent staining.
The role of extracellular vesicles (EVs) in CL release was investigated.
Echo Biotech Role
Echo Biotech contributed EV isolation and purification; the study also used or cited Exosupur®.
Related platforms: Exoomics®, Research Reagents & Tools
Related services and capabilities: Biofluid EV Isolation & Purification, Research Reagent / Product Supply
Related products or reagents: Exosupur® EV Isolation/Purification Kit
References
Original publication: Restoring cardiolipin homeostasis mitigates cerebral ischemia-reperfusion injury by suppressing ATG5-mediated neuronal autophagy-dependent ferroptosis Journal of advanced research. 2026. DOI: 10.1016/j.jare.2026.03.014. PMID/PMCID: 41831680.