ArticleMolecular therapy : the journal of the American Society of Gene Therapy2022
Neuropeptide Y attenuates cardiac remodeling and deterioration of function following myocardial infarction.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 29 papers, 1 of them a synthesis that pooled it.
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Who cites it
29 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Proteins targeting ischaemic-reperfusion injury and repair after myocardial infarction: a systematic literature review.Cardiovascular research · 2026Pooled it
- NPY promotes macrophage polarization and hepatic fibrogenesis via PI3K/MAPK-dependent neuroimmune mechanisms.Cellular and molecular life sciences : CMLS · 2026Article
- Neuropeptide Y in cancer metastasis and chemoresistance.Neuropeptides · 2026Review
- Multidimensional bibliometric analysis and global trends in the nervous system's role in bone regeneration.Regenerative therapy · 2026Article
- Neuropeptide SP protects against colitis and linked anxiety-like behavior through the putative roles of gut microbiota and metabolite inositol.Nature communications · 2026Article
- Hydrogels loaded with different substances for treating heart failure: a promising therapy.Frontiers in cardiovascular medicine · 2026Review
- Advancements in nanomedicine for modulating ischemic cardiomyopathy therapy.Materials today. Bio · 2025Review
- Modulation of Macrophage Polarization by Traditional Chinese Medicine in HFpEF: A Review of Mechanisms and Therapeutic Potentials.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Selumetinib promotes coronary collateral circulation by inducing M2-like macrophage polarization following myocardial infarction.Acta pharmacologica Sinica · 2025Article
- Article
- Bayliss Starling Prize Lecture 2023: Neuropeptide-Y being 'unsympathetic' to the broken hearted.The Journal of physiology · 2025Article
- Bioelectronic block of stellate ganglia mitigates pacing-induced heterogeneous release of catecholamine and neuropeptide Y in the infarcted pig heart.The Journal of physiology · 2025Article
- Ciliary neurotrophic factor attenuates myocardial infarction-induced oxidative stress and ferroptosis via PI3K/Akt signaling.Journal of molecular histology · 2025Article
- Skeletal interoception and prospective application in biomaterials for bone regeneration.Bone research · 2025Review
- Metabolic remodeling in glioblastoma: a longitudinal multi-omics study.Acta neuropathologica communications · 2024Article
- Intermittent Fasting Targets Osteocyte Neuropeptide Y to Relieve Osteoarthritis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The interplay between T lymphocytes and macrophages in myocardial ischemia/reperfusion injury.Molecular and cellular biochemistry · 2024Review
- Multiomics analysis of canine myocardium after circumferential pulmonary vein ablation: Effect of neuropeptide Y on long-term reinduction of atrial fibrillation.Journal of cellular and molecular medicine · 2024Article
- Article
- Naked Gene Delivery Induces Autophagy for Effective Treatment of Acute Lung Injury in a Mouse Model.International journal of nanomedicine · 2024Article
Corrections and comments
- Erratum issued
- Retracted
Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Plasma levels of neuropeptide Y (NPY) are elevated in patients with acute myocardial infarction (AMI), but its role in AMI remains unclear, which was examined here in NPY wild-type/knockout (WT/KO) mice treated with/without exogenous NPY and its Y1 receptor antagonist (Y1Ra) BIBP 3226. We found that AMI mice lacking NPY developed more severe AMI than WT mice with worse cardiac dysfunction, progressive cardiac inflammation and fibrosis, and excessive apoptosis but impairing angiogenesis. All of these changes were reversed when the NPY KO mice were treated with exogenous NPY in a dose-dependent manner. Interestingly, treatment with NPY also dose dependently attenuated AMI in WT mice, which was blocked by BIBP 3226. Phenotypically, cardiac NPY was de novo expressed by infiltrating macrophages during the repairing or fibrosing process in heart-failure patients and AMI mice. Mechanistically, NPY was induced by transforming growth factor (TGF)-β1 in bone marrow-derived macrophages and signaled through its Y1R to exert its pathophysiological activities by inhibiting p38/nuclear factor κB (NF-κB)-mediated M1 macrophage activation while promoting the reparative M2 phenotype in vivo and in vitro. In conclusion, NPY can attenuate AMI in mice. Inhibition of cardiac inflammation and fibrosis while enhancing angiogenesis but reducing apoptosis may be the underlying mechanisms through which NPY attenuates cardiac remodeling and deterioration of function following AMI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.