Titin and Titin-Associated Proteins in Myocardial Stress-Sensing and Mechanical Dysfunction

摘要: Mechanical stress signals transmitted through the heart walls during hemodynamic loading are sensed by myocytes. These play an important role in physiological development and hypertrophy, but disruption of well-balanced stress-sensing machinery causes mechanical dysregulation, cardiac remodelling, failure. In cardiomyocytes, nodal points force transmission mechanosensing reside Z-disk, M-band, I-band regions sarcomeres. Longitudinal linkage these is provided titin filament several “hot spots” along this giant protein may be, with some its > 20 ligands, pivotal to myofibrillar stretch response. This review outlines known interaction partners highlights putative stress/stretch sensor complexes at titin’s NH2 COOH termini their myopathies. Another focus elastic section, which interacts a diverse number proteins whose main function as determinant diastolic distensibility passive stiffness. The discussion summarizes recent insights into plasticity, role, regulation springs human disease. Titin titin-based now recognized integral parts mechanosensitive network critical components cardiomyocyte signalling.