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Heart muscle contraction is regulated via the β-adrenergic response that leads to phosphorylation of Troponin I (TnI) at Ser22/23, which changes the Ca(2+) sensitivity of the cardiac myofilament. Mutations in thin filament proteins that cause dilated cardiomyopathy (DCM) and some mutations that cause hypertrophic cardiomyopathy (HCM) abolish the relationship between TnI phosphorylation and Ca(2+) sensitivity (uncoupling). Small molecule Ca(2+) sensitizers and Ca(2+) desensitizers that act upon troponin alter the Ca(2+) sensitivity of the thin filament, but their relationship with TnI phosphorylation has never been studied before.

Uncoupling of myofilament Ca2+sensitivity from troponin I phosphorylation by mutations can be reversed by epigallocatechin-3-gallate

Uncoupling of myofilament Ca²⁺sensitivity from troponin I phosphorylation by mutations can be reversed by epigallocatechin-3-gallate