The heart undergoes structural changes in response to injury or increased mechanical stress that can contribute to heart failure. Researchers identified the neuropeptide neurotensin (NTS), produced by lymphatic endothelial cells in the injured heart, as an endogenous inhibitor of cardiac hypertrophy and fibrosis acting through neurotensin receptor 2 (NTSR2).
In mouse models of pressure overload and myocardial infarction, the NTSR2 agonist NT150 reduced adverse cardiac remodeling and improved cardiac function. Experiments with human heart tissue supported the protective signaling mechanism. The findings identify NTSR2 as a potential therapeutic target for preventing adverse cardiac remodeling and treating heart failure.
Link to the publication:
Shiva N, Kawase H, Einsiedel J, et al. Neurotensin receptor 2 agonism attenuates adverse cardiac remodeling in preclinical models. Sci Transl Med. 2026;18(856). doi: 10.1126/scitranslmed.aea9877
