
Redox Biology, Journal Year: 2025, Volume and Issue: unknown, P. 103622 - 103622
Published: March 1, 2025
Stroke is known for its high disability and mortality rates. Ischemic stroke (IS), the most prevalent form, imposes a considerable burden on affected individuals. Nevertheless, existing treatment modalities are hindered by limitations, including narrow therapeutic windows, substantial adverse effects, suboptimal neurological recovery. Clarifying pathological mechanism of IS prerequisite developing new strategies. In this context, functional disruption mitochondria, endoplasmic reticulum (ER), crosstalk mechanisms between them have garnered increasing attention their contributory roles in progression IS. Therefore, review provides comprehensive summary current pathomechanisms associated with involvement ER mitochondria IS, emphasising Ca2+ destabilization homeostasis, stress, oxidative disordered mitochondrial quality control, transfer. Additionally, article highlights interaction as well mitochondrial-ER contacts (MERCs) that structurally connect ER, aiming to provide ideas references research
Language: Английский