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Reduction of P62/SQSTM1 on Calcium Handling in Stressed Myocytes

Cytosolic protein, p62/SQSTM1, regulates the protein turnover rate, and it interacts with various stress signaling proteins in cells. Accumulations of p62/SQSTM1 have been reported in hearts with cardiomyopathy. We recently reported that p62/SQSTM1 protein deletions reduced beta‐adrenergic response in myocytes and improved chronic ischemia‐induced Calcium (Ca) defect. Here, we studied acute and chronic stress‐induced Ca handling in myocytes genetically suppressed p62/SQSTM1 protein.