Why the study?
Empagliflozin reduces cardiovascular death or heart failure hospitalization regardless of ejection fraction, but the underlying mechanisms remain to be elucidated.
Does empagliflozin improve Ang II-induced left ventricular dysfunction and microvascular rarefaction in mice and CMECs?
Population
C57BL/6J mice infused with saline or Ang II and primary CMECs
Comparison
EMPA vs no EMPA
Design
In vivo animal and in vitro cell experimental study
Follow-up
2 weeks
Key result
Empagliflozin attenuated Angiotensin II-induced left ventricular dysfunction, microvascular rarefaction, and endothelial-to-mesenchymal transition via the PI3K/AKT/eNOS signaling pathway.
Authors
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Clinical practice should not change; leaves open empagliflozin's therapeutic potential in human HF with microvascular dysfunction.
Does empagliflozin improve Ang II-induced left ventricular dysfunction and microvascular rarefaction in mice and CMECs?
Empagliflozin protects against Ang II-induced left ventricular dysfunction and microvascular rarefaction by suppressing EndoMT via PI3K/AKT/eNOS signaling.
Shen et al. (2026) studied Angiotensin II-induced left ventricular diastolic dysfunction. Empagliflozin vs. Saline or Angiotensin II without Empagliflozin was evaluated on Left ventricular dysfunction, microvascular rarefaction, and endothelial-to-mesenchymal transition (EndoMT). Empagliflozin attenuated Angiotensin II-induced left ventricular dysfunction, microvascular rarefaction, and endothelial-to-mesenchymal transition via the PI3K/AKT/eNOS signaling pathway.