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attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading in cardiomyocytes. | LitMetric

AI Article Synopsis

Article Abstract

Radiation-induced heart disease (RIHD) is a severe delayed complication of thoracic irradiation (IR). Endonuclease/exonuclease/phosphatase family domain-containing 1 ( ) plays an important role in DNA damage repair, but its role in RIHD is less known. In this study, global knockout mice, C57BL/6J mice, and C57BL/6J mice overexpressing are treated with radiation at a total dose of 20 Gy or 0 Gy. After 9 weeks, echocardiography is used to assess cardiac hypertrophy and apoptosis. The results show that deletion exacerbates radiation-induced cardiac hypertrophy and apoptosis, while overexpression has the opposite effect. Further mechanistic investigations reveal that interacts with and destabilizes it by catalyzing its deubiquitination. Inhibition of ameliorates cardiac hypertrophy and apoptosis after knockdown. Thus, protects against radiation-induced cardiac hypertrophy and apoptosis via destabilization of , which may offer new insight into therapeutic strategies for RIHD.

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Source
http://dx.doi.org/10.3724/abbs.2024130DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11659772PMC

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