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It plays a critical role in regulating cellular signaling transduction, maintaining protein stability, and influencing the development of various diseases. This study revealed that USP20 expression was significantly upregulated in transverse aortic constriction (TAC)\u2013induced hypertrophic hearts and in angiotensin II (AngII)\u2013stimulated neonatal rat cardiomyocytes (NRCMs). This study aims to investigate the potential protective role of USP20 deficiency in pressure overload\u2010induced cardiac hypertrophy and to elucidate the underlying molecular mechanisms. Pathological cardiac hypertrophy was induced in mice via transverse aortic constriction (TAC) surgery. Following the procedure, relevant groups of mice were administered shUSP20 adenovirus via tail vein injection, with the TAC intervention lasting 28\u2009days. The results showed that USP20 significantly exacerbated TAC\u2010induced cardiomyocyte apoptosis and inflammatory responses, while simultaneously impairing cardiac function and aggravating myocardial hypertrophy. In\u00a0vitro experiments further confirmed that USP20 markedly aggravated angiotensin II (AngII)\u2013induced cardiomyocyte hypertrophy. Moreover, USP20 enhanced inflammatory responses and apoptosis levels in hypertrophic myocardium, as evidenced by increased levels of Bax, TNF\u2010\u03b1, IL\u20106, and IL\u20101\u03b2, along with a decrease in Bcl2. Mechanistically, USP20 elevated the phosphorylation level of P65, and the protective effect of USP20 knockdown against AngII\u2010induced cellular hypertrophy was further enhanced by co\u2010treatment with the NF\u2010\u03baB inhibitor Bay11\u20107082. USP20 exacerbates cardiac hypertrophy by promoting P65 phosphorylation, which subsequently enhances the release of inflammatory cytokines and apoptotic proteins.<\/jats:p>","DOI":"10.1096\/fj.202600428r","type":"journal-article","created":{"date-parts":[[2026,6,10]],"date-time":"2026-06-10T15:22:47Z","timestamp":1781104967000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["The Deficiency of\n                    <scp>USP20<\/scp>\n                    Alleviates Pressure Overload\u2010Induced Cardiac Hypertrophy via the\n                    <scp>NF<\/scp>\n                    \u2010\n                    <scp>\u03baB<\/scp>\n                    Signaling Pathway"],"prefix":"10.1096","volume":"40","author":[{"given":"Zujun","family":"Fan","sequence":"first","affiliation":[{"name":"Department of Physiology, the School of Basic Medical Sciences Wenzhou Medical University  Wenzhou China"},{"name":"Department of 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