ArticleResearch (Washington, D.C.)2026
Extracellular Vesicle-Mediated Delivery of Mitochondrial Circular RNA MTCO2 Protects against Cerebral Ischemia by Modulating mPTP-Dependent Ferroptosis.
Article in Research (Washington, D.C.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Ischemic stroke remains a major cause of mortality and long-term disability, with few effective neuroprotective treatments currently available. Ferroptosis, an iron-dependent form of regulated cell death marked by lipid peroxidation, is increasingly recognized as a driver of neuronal damage. However, the mitochondrial mechanisms linking ischemia to ferroptosis remain poorly defined. Here, we identify circMTCO2, a mitochondria-encoded circular RNA (circRNA), as a novel endogenous modulator of neuronal ferroptosis. circMTCO2 expression is dynamically down-regulated following cerebral ischemia/reperfusion in vitro and in vivo. Mechanistically, circMTCO2 interacts with adenine nucleotide translocase 1 (ANT1), a key regulator associated with the mitochondrial permeability transition pore (mPTP), thereby inhibiting mPTP opening and suppressing mitochondrial reactive oxygen species release. Disruption of the binding site abolishes circMTCO2-ANT1 interaction and eliminates the protective effects of circMTCO2. To restore and enhance this intrinsic defense mechanism, we developed a dual-targeting extracellular vesicle system (RVG-EV
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