IndraLab

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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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"Furthermore, OTUD7B deficiency exacerbated transverse aortic coarctation surgery-induced myocardial hypertrophy, abnormal cardiac function, and fibrosis."

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"In cardiac myocytes, OTUD7B knockdown promoted phenylephrine stimulation-induced myocardial hypertrophy, whereas OTUD7B overexpression had the opposite effect."

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"Our animal experiments revealed that Cezanne overexpression in mice reversed DOX-induced cardiomyocyte apoptosis, autophagy, oxidative stress and hypertrophy."

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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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"OTUD7B knockdown causes a reprogramming of fatty acid metabolism in pathological cardiac hypertrophy."