Fig. 1.

AF induces a calcium overload in cardiomyocytes, which activates calcium-dependent neutral protease calpain. Calpain degrades contractile proteins and microtubule network resulting in structural remodeling, contractile dysfunction of cardiomyocytes, and AF progression. Elevated HSPB1 is found to inhibit calpain activity in tachypaced Drosophila. In addition, HSPB1 prevents degradation of cardiac troponins and may protect against depolymerization of α-tubulin by sequestering the proteolytic cleavage sites from calpain