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FGF13 Is a Novel Regulator of NF-?B and Potentiates Pathological Cardiac Hypertrophy.


ABSTRACT: FGF13 is an intracellular FGF factor. Its role in cardiomyopathies has been rarely investigated. We revealed that endogenous FGF13 is up-regulated in cardiac hypertrophy accompanied by increased nuclear localization. The upregulation of FGF13 plays a deteriorating role both in hypertrophic cardiomyocytes and mouse hearts. Mechanistically, FGF13 directly interacts with p65 by its nuclear localization sequence and co-localizes with p65 in the nucleus in cardiac hypertrophy. FGF13 deficiency inhibits NF-?B activation in ISO-treated NRCMs and TAC-surgery mouse hearts, whereas FGF13 overexpression shows the opposite trend. Moreover, FGF13 overexpression alone is sufficient to activate NF-?B in cardiomyocytes. The interaction between FGF13 and p65 or the effects of FGF13 on NF-?B have nothing to do with I?B. Together, an I?B-independent mechanism for NF-?B regulation has been revealed in cardiomyocytes both under basal and stressful conditions, suggesting the promising application of FGF13 as a therapeutic target for pathological cardiac hypertrophy and heart failure.

SUBMITTER: Sun J 

PROVIDER: S-EPMC7567043 | BioStudies | 2020-01-01

REPOSITORIES: biostudies

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