Related Experiment Video
Updated: Jun 14, 2025

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
Published on: August 8, 2022
Focus on cardiac troponin complex: From gene expression to cardiomyopathy
Rosetta Ragusa1, Chiara Caselli1,2
1Institute of Clinical Physiology, CNR, via Moruzzi 1, Pisa 56124, Italy.
Abstract:
The cardiac troponin complex (cTn) is a regulatory component of sarcomere. cTn consists of three subunits: cardiac troponin C (cTnC), which confers Ca2+ sensitivity to muscle; cTnI, which inhibits the interaction of cross-bridge of myosin with thin filament during diastole; and cTnT, which has multiple roles in sarcomere, such as promoting the link between the cTnI-cTnC complex and tropomyosin within the thin filament and influencing Ca2+ sensitivity of cTn and force development during contraction. Conditions that interfere with interactions within cTn and/or other thin filament proteins can be key factors in the regulation of cardiac contraction. These conditions include alterations in myofilament Ca2+ sensitivity, direct changes in cTn function, and triggering downstream events that lead to adverse cardiac remodeling and impairment of heart function. This review describes gene expression and post-translational modifications of cTn as well as the conditions that can adversely affect the delicate balance among the components of cTn, thereby promoting contractile dysfunction.
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