Decreased proteasome function increases oxidative stress in the early stage of pressure ulcer development

• DOI: 10.1016/j.yexmp.2024.104891
• Publication Date: 2024-03-22T07:26:55Z
• Authors: Eri Murata; Takuma Yoshida; Utano Tomaru; Saaki Yamamoto; Aya Fukui-Miyazaki; Akihiro Ishizu; Masanori Kasahara

The aging process in the elderly results heightened skin fragility associated with various disorders, including pressure ulcers (PUs). Despite high incidence of PUs population, there is a limited body research specifically examining impact on development ulcers. Therefore, investigating age-related physiological abnormalities essential to elucidate pathogenesis PUs. Ischemia-reperfusion (I/R) injury and subsequent oxidative stress caused by reactive oxygen species (ROS) play roles early stage In this study, we used mouse model proteasomal dysfunction an phenotype examine role proteasome activity cutaneous I/R vivo. Decreased function did not affect expression inflammatory cytokines adhesion molecules area transgenic mice; however, inhibition increased that was attenuated activation response mediated NF-E2-related factor 2 (Nrf2). dermal fibroblasts (FCs) subjected hypoxia-reoxygenation (H/R), induced ROS production, Nrf2 adequately upregulate antioxidant enzyme expression, possibly leading antioxidant/oxidant imbalance. free radical scavenger edaravone had protective effects against vivo decreased FCs treated inhibitor H/R vitro. suggest decline promotes injury-induced stress, scavengers may exert preventing