Neuropeptide Y attenuates cardiac remodeling and deterioration of function following myocardial infarction

• DOI: 10.1016/j.ymthe.2021.10.005
• Publication Date: 2021-10-09T09:18:24Z
• Authors: Yu-Yan Qin; Xiao-Ru Huang; Jian Zhang; Wenjing Wu; Junzhe Chen; Song Wan; Xi-Yong Yu; Hui-Yao Lan
• Keywords: Cardiac Fibrosis; Knockout mouse

Plasma levels of neuropeptide Y (NPY) are elevated in patients with acute myocardial infarction (AMI), but its role AMI remains unclear, which was examined here NPY wild-type/knockout (WT/KO) mice treated with/without exogenous and Y1 receptor antagonist (Y1Ra) BIBP 3226. We found that lacking developed more severe than WT worse cardiac dysfunction, progressive inflammation fibrosis, excessive apoptosis impairing angiogenesis. All these changes were reversed when the KO a dose-dependent manner. Interestingly, treatment also dose dependently attenuated mice, blocked by Phenotypically, de novo expressed infiltrating macrophages during repairing or fibrosing process heart-failure mice. Mechanistically, induced transforming growth factor (TGF)-β1 bone marrow-derived signaled through Y1R to exert pathophysiological activities inhibiting p38/nuclear κB (NF-κB)-mediated M1 macrophage activation while promoting reparative M2 phenotype vivo vitro. In conclusion, can attenuate Inhibition fibrosis enhancing angiogenesis reducing may be underlying mechanisms attenuates remodeling deterioration function following AMI.