Key result
HDAC inhibition with SAHA improved LV relaxation and preserved lung structure, compliance, and blood oxygenation in a feline model of diastolic dysfunction (P<0.01).
Why the study?
Does HDAC inhibition with SAHA improve cardiopulmonary function in a feline model of diastolic dysfunction?
Does HDAC inhibition with SAHA improve cardiopulmonary function in a feline model of diastolic dysfunction?
p-value: p=<0.01
HDAC inhibition with SAHA improves cardiopulmonary function and reverses acetylation defects in a feline model of diastolic dysfunction, suggesting a potential therapeutic target for hypertrophic stress.
SAHA benefits cardiopulmonary function in feline diastolic dysfunction; hypothesis-generating for HDAC inhibition in human HFpEF, requiring clinical trials.
< 0.01) versus b + veh. SAHA increased myofibril relaxation ex vivo, which correlated with in vivo improvements of LV relaxation. Furthermore, SAHA treatment preserved lung structure, compliance, blood oxygenation, and reduced perivascular fluid cuffs around extra-alveolar vessels, suggesting attenuated alveolar capillary stress failure. Acetylation proteomics revealed that SAHA altered lysine acetylation of mitochondrial metabolic enzymes. These results suggest that acetylation defects in hypertrophic stress can be reversed by HDAC inhibitors, with implications for improving cardiac structure and function in patients.
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Wallner et al. (2020) studied Diastolic dysfunction. SAHA (HDAC inhibitor) vs. Vehicle was evaluated on Cardiopulmonary function (LV relaxation, lung structure, compliance, blood oxygenation) (p=<0.01). HDAC inhibition with SAHA improved LV relaxation and preserved lung structure, compliance, and blood oxygenation in a feline model of diastolic dysfunction (P<0.01).
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