Salt inducible kinases (SIKs) are key regulators of cellular metabolism and growth, but their role in cardiomyocyte plasticity and heart failure pathogenesis remains unknown. Here, we showed that loss of SIK1 kinase activity protected against adverse cardiac remodeling and heart failure pathogenesis in rodent models and human iPSC-derived cardiomyocytes. We found that SIK1 phosphorylated and stabilized histone deacetylase 7 (HDAC7) protein during cardiac stress, an event that is required for pathologic cardiomyocyte remodeling. Gain- and loss-of-function studies of HDAC7 in cultured cardiomyocytes implicated HDAC7 as a pro-hypertrophic signaling effector that can induce c-Myc expression, indicating a functional departure from the canonical MEF2 co-repressor function of class IIa HDACs. Taken together, our findings reveal what we believe to be a previously unrecognized role for a SIK1-HDAC7 axis in regulating cardiac stress responses and implicate this pathway as a potential target in human heart failure.
Cerebellar Parieto-occipital Posterior Reversible Encephalopathy Syndrome and Cerebral Metamorphopsia Associated with Asymptomatic Atrial Septum Vegetation and Renal Disease: Case Report.
June 11, 2020
February 25, 2020
Calculation of Stop ages for Colorectal Cancer Screening Based on Comorbidities and Screening History.
May 26, 2020
- ACC 2020The American College of Cardiology decided to cancel ACC.20/WCC due to COVID-19, which was scheduled to take place March 28-30 in Chicago. However, ACC.20/WCC Virtual Meeting continues to release cutting edge science and practice changing updates for cardiovascular professionals on demand and free through June 2020.
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