ArticlePflugers Archiv : European journal of physiology2015
Sexual dimorphic response to exercise in hypertrophic cardiomyopathy-associated MYBPC3-targeted knock-in mice.
Article in Pflugers Archiv : European journal of physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Experimental Models of Hypertrophic Cardiomyopathy: A Systematic Review.JACC. Basic to translational science · 2025Review
- Definitional Challenges in Understanding Hypertrophic Cardiomyopathy.Diagnostics (Basel, Switzerland) · 2024Review
- The carbon monoxide prodrug oCOm-21 increases CaPhysiological reports · 2024Article
- Western diet triggers cardiac dysfunction in heterozygousJournal of molecular and cellular cardiology plus · 2023Article
- Mechano-energetic uncoupling in hypertrophic cardiomyopathy: Pathophysiological mechanisms and therapeutic opportunities.Journal of molecular and cellular cardiology plus · 2023Review
- Ion Channel Impairment and Myofilament CaCells · 2021Review
- Mutation location of HCM-causing troponin T mutations defines the degree of myofilament dysfunction in human cardiomyocytes.Journal of molecular and cellular cardiology · 2021Article
- Proteomic and Functional Studies Reveal Detyrosinated Tubulin as Treatment Target in Sarcomere Mutation-Induced Hypertrophic Cardiomyopathy.Circulation. Heart failure · 2021Article
- Hypertrophic Cardiomyopathy: A Vicious Cycle Triggered by Sarcomere Mutations and Secondary Disease Hits.Antioxidants & redox signaling · 2019Review
- Impact of Demographic Features, Lifestyle, and Comorbidities on the Clinical Expression of Hypertrophic Cardiomyopathy.Journal of the American Heart Association · 2017Review
- Genotype-specific pathogenic effects in human dilated cardiomyopathy.The Journal of physiology · 2017Article
- Diltiazem prevents stress-induced contractile deficits in cardiomyocytes, but does not reverse the cardiomyopathy phenotype in Mybpc3-knock-in mice.The Journal of physiology · 2017Article
- Sex Differences in Metabolic Cardiomyopathy.Cardiovascular research · 2017Article
- Cardiomyocyte Hypocontractility and Reduced Myofibril Density in End-Stage Pediatric Cardiomyopathy.Frontiers in physiology · 2017Article
- Nebivolol Desensitizes Myofilaments of a Hypertrophic Cardiomyopathy Mouse Model.Frontiers in physiology · 2017Article
- Sex dimorphisms of crossbridge cycling kinetics in transgenic hypertrophic cardiomyopathy mice.American journal of physiology. Heart and circulatory physiology · 2016Article
- The Importance of Biological Sex and Estrogen in Rodent Models of Cardiovascular Health and Disease.Circulation research · 2016Review
- Epigallocatechin-3-Gallate Accelerates Relaxation and CaFrontiers in physiology · 2016Article
- Haploinsufficiency of MYBPC3 exacerbates the development of hypertrophic cardiomyopathy in heterozygous mice.Journal of molecular and cellular cardiology · 2015Article
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypertrophic cardiomyopathy (HCM), the most common genetic cardiac disorder, is frequently caused by mutations in MYBPC3, encoding cardiac myosin-binding protein C (cMyBP-C). Moreover, HCM is the leading cause of sudden cardiac death (SCD) in young athletes. Interestingly, SCD is more likely to occur in male than in female athletes. However, the pathophysiological mechanisms leading to sex-specific differences are poorly understood. Therefore, we studied the effect of sex and exercise on functional properties of the heart and sarcomeres in mice carrying a MYBPC3 point mutation (G > A transition in exon 6) associated with human HCM. Echocardiography followed by isometric force measurements in left ventricular (LV) membrane-permeabilized cardiomyocytes was performed in wild-type (WT) and heterozygous (HET) knock-in mice of both sex (N = 5 per group) in sedentary mice and mice that underwent an 8-week voluntary wheel-running exercise protocol. Isometric force measurements in single cardiomyocytes revealed a lower maximal force generation (F max) of the sarcomeres in male sedentary HET (13.0 ± 1.1 kN/m(2)) compared to corresponding WT (18.4 ± 1.8 kN/m(2)) male mice. Exercise induced a higher F max in HET male mice, while it did not affect HET females. Interestingly, a low cardiac troponin I bisphosphorylation, increased myofilament Ca(2+)-sensitivity, and LV hypertrophy were particularly observed in exercised HET females. In conclusion, in sedentary animals, contractile differences are seen between male and female HET mice. Male and female HET hearts adapted differently to a voluntary exercise protocol, indicating that physiological stimuli elicit a sexually dimorphic cardiac response in heterozygous MYBPC3-targeted knock-in mice.
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