fig1
Figure 1. Hypercontractility is central to the pathophysiology of hypertrophic cardiomyopathy. Sarcomere proteins are affected by mutations, redox modifications, and hypophosphorylation, imposing a multitude of functional consequences on the myofilaments. These lead to hypercontractility, increasing adenosine triphosphate (ATP) consumption and raising mitochondrial workload. Sustained elevated mitochondrial workload causes oxidative stress, inducing activation of hypertrophic and fibrotic pathways. Created in BioRender. Nollet E. (2025) https://BioRender.com/ntotvnr. SRX: Super-relaxed myosin; DRX: disordered-relaxed myosin; β-AR:
