In renal proximal tubular epithelial cells of the hibernator Syrian hamster, anoxia-reoxygenation-induced reactive oxygen species bursts do not trigger a DNA damage response and cellular senescence.

ABSTRACT: Ischemia-reperfusion (I-R) injury represents a predominant etiology of acute kidney injury (AKI), for which effective treatments remain unavailable. In contrast, hibernating mammals exhibit notable resistance to cell death induced by I-R injury. However, the impact of I-R injury on cellular senescence-an important factor in AKI-has not been extensively studied in these species. Comparative biology may offer novel therapeutic insights. Renal proximal tubular epithelial cells (RPTECs) from the native hibernator Syrian hamster or mouse RPTECs were subjected to anoxia-reoxygenation. Proteins involved in DNA damage response (DDR) and cellular senescence were assessed using western blotting, reactive oxygen species (ROS) levels and cell death were quantified colorimetrically, and IL-6 with ELISA

SUBMITTER: Pissas G 

PROVIDER: S-EPMC11839863 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature