Key result
Titin acts as a versatile and adjustable molecular spring that modulates myocardial passive stiffness, actomyosin interaction, and links to membrane channels, protein turnover, and gene expression.
This review highlights the multifaceted roles of the giant elastic protein titin in both passive and contracting myocardium, extending beyond simple passive stiffness generation.
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Titin modulation may inform diastolic HF therapies; leaves open clinical translation pending targeted studies.
The giant elastic protein titin contains a molecular spring segment that underlies the majority of myocardial passive stiffness. The mechanical characteristics of this spring may be tuned to match changing mechanical demands placed on muscle, using mechanisms that operate on different time scales and that include post-transcriptional and post-translational processes. Recent work also suggests that titin performs roles that go beyond passive stiffness generation. In contracting myocardium, titin may modulate actomyosin interaction by a titin-based alteration of the distance between myosin heads and actin. Furthermore, novel ligands have been identified that link titin to membrane channels, protein turnover and gene expression. This review highlights that titin is a versatile and adjustable spring with a range of important functions in passive and contracting myocardium.
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Granzier et al. (2002) conducted a review in Myocardial function. Titin was evaluated. Titin acts as a versatile and adjustable molecular spring that modulates myocardial passive stiffness, actomyosin interaction, and links to membrane channels, protein turnover, and gene expression.
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