Answers are grounded in this paper and cite their sources.
This review highlights the role of e3 ubiquitin ligases in ischemia-reperfusion injury, indicating their potential as therapeutic targets for improving outcomes.
The temporary or permanent occlusion of cerebral blood vessels results in ischemic stroke (IS). Ischemia per se causes focal neuronal damage, and the subsequent ischemia–reperfusion injury that occurs after blood flow restoration further compromises brain tissue and cells in the neurovascular unit, significantly contributing to poor patient outcomes and functional impairments. Current research indicates that the ubiquitin–proteasome system (UPS) plays a crucial role in the pathological processes associated with cerebral ischemia–reperfusion injury (CIRI). Notably, E3 ubiquitin (Ub) ligases, which are essential in the UPS, have garnered increasing attention as potential novel therapeutic targets for treating ischemia–reperfusion damage in the brain. This review focuses primarily on the background of E3 Ub ligases and explores their intricate relationships with the pathological processes of CIRI.
No takes yet. Share an insight, caveat, or question.
Li et al. (2025) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: