Cuproptosis in Ischemic Stroke: Molecular Mechanisms and Therapeutic Potential
TL;DR
The molecular mechanisms of cuproptosis and its potential involvement in cerebral ischemia are summarized, and the therapeutic potential of cuproptosis-targeting agents for improving neurological outcomes after stroke is discussed.
Abstract
Stroke is a major neurological disease caused by cerebral vascular obstruction or rupture and represents a leading cause of death and long-term disability worldwide. Ischemic stroke (IS) accounts for the majority of stroke cases, while effective therapeutic strategies remain limited. Therefore, a better understanding of the underlying pathological mechanisms and the identification of new therapeutic targets are urgently needed. Cerebral ischemia triggers various regulated forms of cell death, including apoptosis, ferroptosis, and cuproptosis, which was discovered in recent years. Emerging evidence suggests that copper imbalance and copper-dependent cell death may play important roles in the development and progression of IS. This review summarizes the molecular mechanisms of cuproptosis and its potential involvement in cerebral ischemia, and discusses the therapeutic potential of cuproptosis-targeting agents for improving neurological outcomes after stroke.