The cardiac troponin complex (cTn) is a regulatory component of sarcomere. cTn consists of three subunits: cardiac troponin C (cTnC), which confers Ca 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 Ca 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 Ca 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.

中文翻译：

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关注心肌肌钙蛋白复合物：从基因表达到心肌病

心肌肌钙蛋白复合物 (cTn) 是肌节的调节成分。cTn 由三个亚基组成：心肌肌钙蛋白 C (cTnC)，赋予肌肉 Ca 敏感性；cTnI，抑制舒张期肌球蛋白与细丝的跨桥相互作用；cTnT 在肌节中具有多种作用，例如促进细丝内 cTnI-cTnC 复合物和原肌球蛋白之间的联系，影响 cTn 的 Ca 敏感性和收缩过程中的力发展。干扰 cTn 和/或其他细丝蛋白内相互作用的条件可能是调节心脏收缩的关键因素。这些情况包括肌丝 Ca 敏感性的改变、cTn 功能的直接变化以及触发导致不良心脏重塑和心脏功能受损的下游事件。这篇综述描述了 cTn 的基因表达和翻译后修饰，以及可能对 cTn 成分之间的微妙平衡产生不利影响的条件，从而促进收缩功能障碍。