Key result
Recent findings highlight titin's role as a molecular spring in cardiac muscle, its function as a biomechanical sensor and signaling molecule, and the growing knowledge regarding titinopathies.
This review highlights the structural and functional roles of the giant protein titin in the heart, including its function as a molecular spring, biomechanical sensor, and its involvement in titinopathies.
Titin's roles merit investigation in unexplained cardiomyopathies; extends sarcomere biology but leaves therapeutic translation open.
The sarcomere contains, in addition to thin and thick filaments, a filament composed of the giant protein titin (also known as connectin). Titin molecules anchor in the Z-disc and extend to the M-line region of the sarcomere. The majority of titin's I-band region functions as a molecular spring. This spring maintains the precise structural arrangement of thick and thin filaments, and gives rise to passive muscle stiffness; an important determinant of diastolic filling. Earlier work on titin has been reviewed before. In this study, our main focus is on recent findings vis-à-vis titin's molecular spring segments in cardiac titins, including the discovery of fetal cardiac isoforms with novel spring elements. We also discuss new insights regarding the role of titin as a biomechanical sensor and signaling molecule. We will end with focusing on the rapidly growing knowledge regarding titinopathies.
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Granzier et al. (2004) conducted a review in Titinopathies. Recent findings highlight titin's role as a molecular spring in cardiac muscle, its function as a biomechanical sensor and signaling molecule, and the growing knowledge regarding titinopathies.
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