{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE335nnn/GSE335342/"]},"type":"primary"},"statusCodeValue":200,"statusCode":"OK"}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Mus musculus"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE335342"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Meteorin-like regulates cardiac repair via macrophage modulation following myocardial infarction","description":"After myocardial infarction (MI), the heart undergoes a reparative process that includes an initial acute inflammatory phase followed by a subsequent reparative phase. The transition between these phases is crucial for cardiac recovery, but the key factors remain unclear. Meteorin-like (Metrnl) promotes anti-inflammatory macrophage polarization in the myocardium, yet its role in the acute phase post-MI is unknown. We observed that macrophages infiltrating the ischemic myocardium produced elevated levels of Metrnl in both the heart and circulation 4 days post-MI. The absence of Metrnl in Metrnl⁻/⁻ mice altered myocardial healing and remodeling, with an increased presence of macrophages with a more pro-inflammatory phenotype. Conversely, cardiac Metrnl overexpression restored myocardial repair and promoted a shift toward a more anti-inflammatory macrophage phenotype. Mechanistically, Metrnl regulated macrophage-dependent production of Oncostatin M (Osm), a key cytokine in the early inflammatory phase post- MI that induces cardiomyocyte production of Reg3β. Reg3β, in turn, limits classical macrophage activation and polarization while modulating their trafficking, ultimately influencing the duration and intensity of the pro-inflammatory phase post-MI. Thus, Metrnl plays a crucial role in cardiac repair by modulating the acute phase following myocardial infarction through its regulation of macrophage populations.","dates":{"publication":"2026/08/03"},"accession":"GSE335342","cross_references":{"GSM":["GSM9812255","GSM9812254","GSM9812256","GSM9812251","GSM9812253","GSM9812252"],"GPL":["34290"],"GSE":["335342"],"taxon":["Mus musculus"],"PMID":["[42536170]"]}}