Key result
Long-term volume overload induces heart failure driven by decreased Akt, increased CaMKII, and oxidative stress.
Why the study?
Does long-term volume overload induce heart failure through specific molecular and structural transition mechanisms in mice?
Does long-term volume overload induce heart failure through specific molecular and structural transition mechanisms in mice?
Long-term volume overload induces heart failure through decreased Akt and increased CaMKII signaling, leading to sarcomeric stiffness rather than matrix fibrosis.
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Hypothesis-generating for titin-targeted therapies in volume-overload HF; requires human validation before clinical consideration.
Mohamed et al. (2015) studied Volume overload-induced heart failure. Volume overload (aortocaval shunt) vs. Sham was evaluated on Heart failure development (LVEF <50%). Long-term volume overload induced heart failure (LVEF <50%) at 135 ± 35 days, driven by decreased Akt signaling, increased CaMKII, oxidative stress, and sarcomeric titin hypophosphorylation.
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