Cellular & Molecular Biology Letters, Год журнала: 2025, Номер 30(1)

Опубликована: Апрель 7, 2025

Abstract Ischemia–reperfusion (I/R) injury describes the pathological process wherein tissue damage, initially caused by insufficient blood supply (ischemia), is exacerbated upon restoration of flow (reperfusion). This phenomenon can lead to irreversible damage and commonly observed in contexts such as cardiac surgery stroke, where temporarily obstructed. During ischemic conditions, anaerobic metabolism tissues organs results compromised enzyme activity. Subsequent reperfusion exacerbates mitochondrial dysfunction, leading increased oxidative stress accumulation reactive oxygen species (ROS). cascade ultimately triggers cell death through mechanisms autophagy mitophagy. Autophagy constitutes a crucial catabolic mechanism within eukaryotic cells, facilitating degradation recycling damaged, aged, or superfluous organelles proteins via lysosomal pathway. essential for maintaining cellular homeostasis adapting diverse conditions. As self-degradation clearance mechanism, exhibits dualistic function: it confer protection during initial phases injury, yet potentially exacerbate later stages. paper aims elucidate fundamental I/R highlighting its dual role regulation effects on both organ-specific systemic responses. By comprehending their implications organ function, this study seeks explore potential therapeutic interventions modulation clinical settings.

Язык: Английский