Organelle regulation of ferroptosis after intracerebral hemorrhage

Intracerebral hemorrhage (ICH) is a devastating form of acute cerebrovascular disease characterized by high mortality and long-term disability, posing a substantial public health burden. Ferroptosis has emerged as a pivotal mechanism underlying secondary brain injury (SBI) after ICH, driven by reactive iron accumulation, amplification of lipid peroxidation (LPO) cascades, and disruption of cellular antioxidant defenses. Despite growing evidence supporting its involvement, the precise regulatory networks governing ferroptosis after ICH remain to be fully clarified. This review integrates recent advances to delineate how mitochondria, the endoplasmic reticulum (ER), lysosomes, lipid droplets (LDs), peroxisomes, the Golgi apparatus, and inter organelle membrane contact sites (MCSs) contribute to ferroptosis after ICH. We further summarize current therapeutic strategies targeting ferroptosis from an organelle-centered perspective and highlight its potential as a promising avenue for future intervention.