Key result
Targeting molecular mechanisms of cardiomyocyte stiffness offers potential new interventions for diastolic heart failure.
Why the study?
As the prevalence of conditions involving diastolic heart failure escalates, a more sophisticated understanding of the molecular, cellular, and tissue determinants of cardiomyocyte stiffness is needed to develop imaging and intervention tools.
Understanding the cellular and molecular determinants of cardiomyocyte stiffness may offer potential for developing new imaging and molecular intervention tools for diastolic heart failure.
No immediate practice change in diastolic HF; leaves open targeted trials on stiffness modulators.
effector in diastole, the myosin ADP dissociation rate as a modulator of cross bridge attachment and regulation of cross-bridge attachment by myosin binding protein C. We also discuss non-cross bridge-derived stiffness sources, including the titin sarcomeric spring protein, microtubule and intermediate filaments, and cytoskeletal extracellular matrix interactions. As the prevalence of conditions involving diastolic heart failure has escalated, a more sophisticated understanding of the molecular, cellular, and tissue determinants of cardiomyocyte stiffness offers potential to develop imaging and molecular intervention tools.
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Janssens et al. (2024) conducted a review in Diastolic dysfunction and diastolic heart failure. Understanding the molecular and cellular determinants of cardiomyocyte stiffness, including cross-bridge and non-cross-bridge sources, offers potential for developing new interventions for diastolic heart failure.
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