Focus on cardiac troponin complex: From gene expression to cardiomyopathy

被引:2
作者
Ragusa, Rosetta [1 ]
Caselli, Chiara [1 ,2 ]
机构
[1] CNR, Inst Clin Physiol, Via Moruzzi 1, I-56124 Pisa, Italy
[2] Fdn Toscana Gabriele Monasterio, Via Moruzzi 1, I-56124 Pisa, Italy
关键词
Cardiac troponin; Cardiomyopathy; Gene mutation; Post-translational modification; Therapy; FAMILIAL HYPERTROPHIC CARDIOMYOPATHY; MUSCLE THIN FILAMENT; MYOFILAMENT CALCIUM SENSITIVITY; MYOCARDIAL OXYGEN-CONSUMPTION; DILATED CARDIOMYOPATHY; I PHOSPHORYLATION; FUNCTIONAL-CHARACTERIZATION; CA2+ SENSITIVITY; T MUTATIONS; RESTRICTIVE CARDIOMYOPATHY;
D O I
10.1016/j.gendis.2024.101263
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The cardiac troponin complex (cTn) is a regulatory component of sarcomere. cTn consists of three subunits: cardiac troponin C (cTnC), which confers Ca2 & thorn; 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 & thorn; 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 & thorn; 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 posttranslational modifications of cTn as well as the conditions that can adversely affect the delicate balance among the components of cTn, thereby promoting contractile dysfunction. (c) 2024 The Authors. Publishing services by Elsevier B.V. on behalf of KeAi Communications Co., Ltd. This is an open access article under the CC BY license (http://creativecommons.org/ licenses/by/4.0/).
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页数:20
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