IndraLab

Statements

OTUD7B inhibits Fibrosis. 5 / 5
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"Gene set enrichment analysis showed that fibrosis, heart function, and protein processing‐related pathways were all activated by OTUD7B deficiency (Figure 5B)."
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"Furthermore, OTUD7B deficiency exacerbated transverse aortic coarctation surgery-induced myocardial hypertrophy, abnormal cardiac function, and fibrosis."
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"Histological examinations using H&E (Fig. 2G), WGA (Fig. 2H), Masson (Fig. 2J, K), and Sirius Red staining (Fig. 2L, M) consistently indicated that OTUD7B knockdown significantly intensified pressure overload-induced cardiac hypertrophy and fibrosis."
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"Collectively, these findings demonstrate that OTUD7B knockdown exacerbates pressure overload-induced myocardial hypertrophy and fibrosis, leading to deteriorated cardiac function."
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"These data provided further evidence that OTUD7B deficiency promotes cardiac remodeling and fibrosis."
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