ArticleJournal of muscle research and cell motility2026
Hypertrophic cardiomyopathy-linked Tnnc1 variants are associated with distinct myopathic changes in slow skeletal muscle of mice.
Article in Journal of muscle research and cell motility, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Inherited hypertrophic cardiomyopathy (HCM) is considered a disease of the cardiac sarcomere and caused by pathogenic variants present in genes that encode sarcomeric proteins. The human TNNC1 gene is a designated HCM-susceptibility gene encoding the troponin C (TnC) protein, which is expressed in both cardiac and type I slow skeletal muscles and abbreviated as cTnC and ssTnC respectively. HCM patients have been reported to exhibit skeletal muscle weakness and reduced exercise tolerance. Patients bearing TNNC1 cardiac pathogenic variants also express it in type I fibers of their slow skeletal muscles. We hypothesized that the presence of TNNC1 HCM variants in type I fibers may decrease force generating capabilities and alter fatigue resistance of slow skeletal muscles. To address this, we examined the impact of HCM Tnnc1 variants in the soleus muscles of two HCM knock-in mouse models A8V+/-, A8V-/-, and C84Y+/- and their respective wild type (WT) controls. At high stimulation frequencies, we found that A8V-/- soleus muscles had lower tetanic force production than WT, however no differences in fatigue when comparing fatigue indices for either of the variants. The muscles were evaluated by comparing % specific force (N/cm
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