Titin functions as a critical mechanosensor in cardiac muscle, translating mechanical stress and strain into biochemical signals that can trigger cardiac hypertrophy.
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Titin mechanosensing may inform hypertrophy pathways; leaves open clinical translation or targeted therapies.
The giant filamentous protein titin is ideally positioned in the muscle sarcomere to sense mechanical stimuli and transform them into biochemical signals, such as those triggering cardiac hypertrophy. In this review, we ponder the evidence for signaling hotspots along the titin filament involved in mechanosensory control mechanisms. On the way, we distinguish between stress and strain as triggers of mechanical signaling events at the cardiac sarcomere. Whereas the Z-disk and M-band regions of titin may be prominently involved in sensing mechanical stress, signaling hotspots within the elastic I-band titin segment may respond primarily to mechanical strain. Common to both stress and strain sensor elements is their regulation by conformational changes in protein domains.
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Voelkel et al. (2011) studied this question.
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