SGLT2 inhibitor empagliflozin curbs cardiac hypertrophy through integrin-dependent signalling
- Empagliflozin was tested for a direct anti-hypertrophic action independent of glucose control, using angiotensin II-stimulated human and rat cardiomyocyte lines and a mouse pressure-overload model.
- It reduced hypertrophy, dysfunction and fibrosis; transcriptomics pointed to extracellular matrix-receptor and focal adhesion pathways, and elevated integrin subunits in diseased hearts were brought back toward normal.
- The integrin blocker ATN-161 abolished the benefit and the FAK/Src/Akt response, indicating integrin dependence, while docking and SP1 knockdown suggested SP1 as a possible link to integrin expression.
💡 Points Based on the abstract
What does the ATN-161 rescue really prove? It's a peptide that hits more than one integrin, so losing the benefit shows integrin involvement, not that empagliflozin acts on integrins directly. Before calling this SGLT2-independent, I'd want in vitro concentrations matched to free clinical exposure and an SGLT2-null or genetic control.
Empagliflozin inhibits cardiac hypertrophy via a mechanism involving integrin signalling ↗