The PKM2 activator TEPP-46 suppresses cellular senescence in hydrogen peroxide-induced proximal tubular cells and kidney fibrosis in CD-1

Shin-Ichiro Ishihara, Md Imrul Kayes, Hirofumi Makino, Hiroaki Matsuda, Asako Kumagai, Yoshihiro Hayashi, Sara Amelia Ferdaus, Emi Kawakita, Daisuke Koya, Keizo Kanasaki

Faculty of Medicine, Internal Medicine, Shimane University, Izumo, Shimane, Japan.Faculty of Medicine, Internal Medicine, Shimane University, Izumo, Shimane, Japan. · pubmed

Paper

Abstract

Senescence is a key driver of age-related kidney dysfunction, including diabetic kidney disease. Oxidative stress activates cellular senescence, induces abnormal glycolysis, and is associated with pyruvate kinase muscle isoform 2 (PKM2) dysfunction; however, the mechanisms linking PK activation to cellular senescence have not been elucidated. We hypothesized that PKM2 activation by TEPP-46 could suppress oxidative stress-induced renal tubular cell injury and cellular senescence.

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Research summary

The paper claims that PKM2 activation by TEPP-46 can suppress oxidative stress-induced renal tubular cell injury and cellular senescence. This research addresses the mechanisms of cellular senescence, which is a key factor in age-related kidney dysfunction, thus contributing to the understanding of aging processes.

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