Phosphorylation and Fragmentation of the Cardiac Troponin T: Mechanisms, Role in Pathophysiology and Laboratory Diagnosis

Abstract

Cardiac troponin T (cTnT), a protein essential for calcium-regulated, myofibrillar ATPase activity, is extremely sensitive to the action of a significant number of intra- and extracellular enzymes, the action of which causes post-translational modifications (PTMs) of amino acid structure and functioning cTnT. PTMs of cTnT may play important roles in the regulation of cardiac contractility. The vast majority of cTnT modifications involve the phosphorylation by a variety of Ser/Thr kinases, including PKC. At the same time, the activity of cTnT phosphorylation can change under physiological conditions and in some CVDs, including HF, AMI, and arrhythmias. Along with cTnT phosphorylation, cTnT fragmentation occurs, the activity of which can also change. This article discusses the mechanisms of cTnT phosphorylation and fragmentation, discusses the important role of these processes in the pathophysiology and laboratory diagnosis of some CVD, and notes promising directions for further research.