Key result
Inhibition of neutrophil extracellular traps via deoxyribonuclease 1, HMGB1 inhibition, or empagliflozin attenuated cardiac fibrosis and improved diastolic function in HFpEF mice.
Why the study?
Heart failure with preserved ejection fraction carries substantial morbidity and mortality with few effective treatments, and the inflammatory signals driving its development remain largely unknown.
Does inhibition of NETs, HMGB1, or treatment with empagliflozin improve diastolic function and reduce cardiac fibrosis in a mouse model of HFpEF?
Population
Patients with HFpEF and male C57BL/6 mice with induced HFpEF phenotype
Comparison
Inhibition of NETs (deoxyribonuclease 1), HMGB1, or SGLT2 (empagliflozin) vs controls
Design
Translational human biomarker study and animal/in vitro mechanistic experiment
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Hypothesis-generating for NET inhibition in HFpEF; leaves open translation to human diastolic dysfunction.
Does inhibition of NETs, HMGB1, or treatment with empagliflozin improve diastolic function and reduce cardiac fibrosis in a mouse model of HFpEF?
HMGB1-promoted neutrophil extracellular traps contribute to HFpEF pathogenesis, and their inhibition or treatment with empagliflozin improves diastolic function in mice.
A 2022 study studied Heart failure with preserved ejection fraction (HFpEF). NETs inhibition (deoxyribonuclease 1), HMGB1 inhibition, and empagliflozin was evaluated on Cardiac fibrosis and diastolic function. Inhibition of neutrophil extracellular traps via deoxyribonuclease 1, HMGB1 inhibition, or empagliflozin attenuated cardiac fibrosis and improved diastolic function in HFpEF mice.
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