IndraLab

Statements

OTUD1 activates Hypertrophy. 11 / 11
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"OTUD1 deficiency attenuated myocardial hypertrophy and cardiac dysfunction induced by ISO infusion or MI operation."
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"The macrophage inflammation mediated by the ISO‐OTUD1‐CARD9 axis further promotes hypertrophy and fibrosis in cardiomyocytes and fibroblasts, respectively, inducing cardiac remodelling."
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"m6A modification leads to OTUD1 upregulation in cardiac hypertrophy."
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"Wang et al. demonstrated that OTUD1 promoted the development of pathological myocardial hypertrophy by removing the K63-linked ubiquitin chains of STAT3 and stabilizing the protein in various rodent models of myocardial hypertrophy."
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"OTUD1 deficiency prevents TAC-induced myocardial hypertrophy and fibrosis."
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"We speculated that OTUD1 might promote cardiac hypertrophy by activating MAPK signaling."
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"these results confirm that OTUD1 deficiency suppresses deleterious myocardial hypertrophy and fibrosis."
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"These results show that OTUD1 is needed for Ang II to induce hypertrophy and expression of fibrotic factors in cardiomyocytes."
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"OTUD1 promotes Cardiac Hypertrophy in an ASK1-Dependent Manner."
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"Our group has recently found that cardiomyocyte OTUD1 promoted angiotensin II‐ and TAC‐driven cardiac dysfunction, hypertrophy and fibrosis, while the role of OTUD1 was evaluated using the whole‐body OTUD1 knockout mice but not the myocardial‐specific OTUD1 knockout mice or BMT."
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"OTUD1 increases Ang II-induced cardiomyocyte myocardial hypertrophy and fibrosis by regulating STAT3."
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