Why the study?
The relative contributions of passive sarcomere stiffness, microtubules, and diastolic crossbridges to cardiomyocyte diastolic stiffness in HFpEF conditions were unclear.
Population
Intact cardiomyocytes isolated from two-hit cardiometabolic HFpEF-like mice of both sexes
Comparison
XB inhibitor, colchicine, or combined treatment vs baseline
Design
Preclinical experimental study
Key result
Male HFpEF-like cardiomyocytes exhibited increases in passive sarcomere stress (by 70%) and diastolic crossbridges (by 52%), whereas female cardiomyocytes showed an increase in passive sarcomere stress alone (by 55%).
Authors
Loading...
Animal models identify diastolic stiffness contributors in HFpEF; leaves open clinical translation and therapeutic targeting.
Sex differences exist in the mechanisms of cardiomyocyte diastolic stiffness in a cardiometabolic HFpEF-like mouse model, with males showing increased passive sarcomere stiffness and diastolic crossbridge activity, while females show only increased passive sarcomere stiffness.
Shahid et al. (2026) studied HFpEF-like mouse model. XB inhibitor and colchicine treatment was evaluated on Relative contributions of passive sarcomere stress, the microtubule network, and diastolic XB activity to overall diastolic stress. Male HFpEF-like cardiomyocytes exhibited increases in passive sarcomere stress (by 70%) and diastolic crossbridges (by 52%), whereas female cardiomyocytes showed an increase in passive sarcomere stress alone (by 55%).