![]() They do this by binding to the Z-disc myofilament anchor proteins, α-actinin and telethonin, and tethering them to calcineurin, a calcium-dependent phosphatase that was shown to directly induce cardiomyocyte hypertrophy by downstream transcriptional pathways. Calsarcins were shown to couple the cardiac skeletal apparatus to signaling molecules that can directly influence gene expression. A good example of mechanosensitive molecules that have gained attention in recent years are a family of Z-disc-specific proteins called calsarcins, also known as myozenins. The sarcomeric Z-disc and its associated proteins have been suggested to drive mechanical stress-induced signal transduction, a process referred to as “mechanotransduction”. Mechanical stress is thought to induce a hypertrophic response downstream of mechanosensitive molecules. Īt the cellular level, cardiomyocyte hypertrophy is characterized by an increase in cell size, enhanced protein synthesis, and heightened organization of the sarcomere. Ventricular hypertrophy is hence considered as a predictor of cardiovascular morbidity and mortality. Additionally, myocardial supply-demand mismatch secondary to increased myocardial oxygen consumption of the hypertrophic heart further predisposes to multiple cardiovascular ailments, including arrhythmias, myocardial infarction, cerebrovascular events, and sudden death. These are foreboding signs of the development heart failure and pathological remodeling. However, in the presence of chronic stressful conditions such as hypertension and valvular disease, a form of pathological hypertrophy develops, which is characterized by excessive increase in ventricular dimensions, accompanied by myocardial dysfunction and fibrosis. Physiological hypertrophy of the heart can ensue as a result of exercise or pregnancy, and is deemed mild and/or reversible. Hypertrophic growth of the heart is an adaptive response to hemodynamic stress, which is believed to have a compensatory role to enhance cardiac performance and diminish ventricular wall tension and oxygen consumption. ![]()
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