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内容記述 |
In summary, recent nano-imaging studies have revealed that the length of each sarcomere does not change in a synchronous fashion throughout excitation-contraction coupling in myocytes in the beating heart in vivo (Kobirumaki-Shimozawa et al., 2016; Kobirumaki-Shimozawa et al., 2021), as well as in cultured (Shintani et al., 2014; Tsukamoto et al., 2016) or isolated cardiomyocytes (Li et al., 2023). Increasing levels of titin-based passive force under depressed conditions enhances dynamic instability between sarcomeres along myofibrils (Kobirumaki-Shimozawa et al., 2021), due presumably to blood congestion in the heart, which is likely to cause marked asynchrony of sarcomere movements and hence progressive exacerbation of myocardial contractility. Previous studies show that the slack SL is similar between myocytes with and without DCM (e.g., Inoue et al., 2013; Beqqali et al., 2016); however, no systematic studies have been conducted to accurately analyze the movements of individual sarcomeres in diseased myocardium, including DCM, under living conditions in vivo. Therefore, future studies are warranted to directly investigate the link between sarcomere asynchrony and cardiac pump function in various heart disease mouse models, especially DCM and congestive heart failure. |
