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"Experiments performed in transgenic mice demonstrated that the increased USP18 expression in cardiomyocytes upon an increased afterload attenuated the cardiomyocyte hypertrophy and myocardial fibrosis, resulting in the delayed development of heart failure."

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"In brief, the authors observed that cardiomyocyte-specific overexpression of USP18 attenuated myocardial hypertrophy, fibrosis, ventricular dilatation, and ejection fraction decline induced by aortic banding, whereas USP18 knockout exacerbated remodeling (59)."

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"USP18 plays a well-described protective role in the development of heart failure but its role in kidney injury remains unrecognized.Both in murine experimental models and in humans, USP18 inhibits myocardial hypertrophy via the TAK1-p38-JNK1/2 axis upon an increased afterload [4]."

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"(p72) , (p73) Ubiquitin-specific protease 18 (USP18) attenuated cardiac hypertrophy by specifically removing the K63-linked polyubiquitination of TAK1, leading to the inactivation of the TAK1-p38/JNK1[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"