Key result
Titin acts as an essential mechanotransduction scaffold and potential therapeutic target for DCM and HFpEF.
Why the study?
This review aims to discuss recent insights into titin's functional roles, their relationship to cardiac function, its role in heart diseases such as DCM and HFpEF, and its potential as a therapeutic target.
Understanding titin's structural and signaling roles provides mechanistic insights into the pathophysiology of dilated cardiomyopathy and heart failure with preserved ejection fraction.
Titin modulation remains investigational; leaves open its viability as a therapeutic target pending clinical trials in cardiomyopathy and HFpEF.
The giant protein titin is an essential component of muscle sarcomeres. A single titin molecule spans half a sarcomere and mediates diverse functions along its length by virtue of its unique domains. The A-band of titin functions as a molecular blueprint that defines the length of the thick filaments, the I-band constitutes a molecular spring that determines cell-based passive stiffness, and various domains, including the Z-disk, I-band, and M-line, serve as scaffolds for stretch-sensing signaling pathways that mediate mechanotransduction. This review aims to discuss recent insights into titin's functional roles and their relationship to cardiac function. The role of titin in heart diseases, such as dilated cardiomyopathy and heart failure with preserved ejection fraction, as well as its potential as a therapeutic target, is also discussed.
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Stroik et al. (2024) conducted a review in Heart diseases (dilated cardiomyopathy, heart failure with preserved ejection fraction). Titin (therapeutic target) was evaluated. Titin serves as an essential molecular spring and scaffold for mechanotransduction in cardiac function, presenting a potential therapeutic target for dilated cardiomyopathy and HFpEF.
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