Key result
Dapagliflozin preserves diastolic function and suppresses cardiac fibrosis and steatosis in an HIV mouse model.
Why the study?
Myocardial fibrosis, steatosis, and HFpEF are increasing among people with HIV, and dapagliflozin is a promising therapy for the inflammatory component of cardiovascular disease risk in this population.
Does dapagliflozin improve diastolic function and reduce cardiac fibrosis and steatosis in a mouse model of HIV?
Does dapagliflozin improve diastolic function and reduce cardiac fibrosis and steatosis in a mouse model of HIV?
Dapagliflozin attenuates HIV-associated cardiac fibrosis, steatosis, and diastolic dysfunction in a mouse model, suggesting potential utility for heart failure with preserved ejection fraction in people with HIV.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for SGLT2i in HIV-associated HFpEF; leaves open efficacy pending human trials.
Myocardial fibrosis, steatosis, and heart failure with preserved ejection fraction are increasing among people with HIV (PWH). The sodium-glucose cotransporter type 2 inhibitor (SGLT2i) dapagliflozin has efficacy for cardiovascular disease (CVD) prevention in type 2 diabetes and is a promising therapy for the inflammatory component of CVD risk in PWH. We show dapagliflozin preserved diastolic function and suppressed cardiac fibrosis and steatosis linked to HIV in mice, suggesting potential utility in PWH.
No takes yet. Share an insight, caveat, or question.
Laurence et al. (2026) studied HIV-associated cardiac fibrosis, steatosis and diastolic dysfunction. Dapagliflozin was evaluated on Diastolic function, cardiac fibrosis, and steatosis. Dapagliflozin preserved diastolic function and suppressed cardiac fibrosis and steatosis in a mouse model of HIV.
Synapse has enriched 10 related papers. Consider them for comparative context: