IndraLab

Statements


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"Overexpression of USP4 can prevent angiotensin II induced cardiac hypertrophy and fibrosis in vitro and ameliorate cardiac dysfunction in vivo through downregulation of the TAK1/JNK1/2/p38 signaling pathway."

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"Adenovirus mediated gain- and loss-of-function approaches indicated that deficiency of endogenous USP4 promoted myocyte hypertrophy induced by angiotensin II in vitro, whereas restoration of USP4 significantly attenuated the prohypertrophic effect of angiotensin II."