{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE174nnn/GSE174547/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"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=GSE174547"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"Vascular mitohormesis couples Mfn2 with improved systemic metabolism and healthspan","description":"In this study, we hypothesized that mitochondrial dynamics in ECs orchestrates whole-body metabolic status. Here we report that genetic deficiency of endothelial Mfn2 (Mfn2iΔEC) in mice, originated a mitohormetic response that caused favorable vascular adaptations with regards to antioxidant defenses, mitochondrial fitness and lipid oxidation. As a result, Mfn2iΔEC mice exhibited improved metabolism, resistance to diet-induced obesity and delayed age-related decline. Our results reveal vascular mitohormesis as a novel operation mode influencing systemic energy metabolism and healthspan. These findings endorse the endothelium as a genuine metabolic organ and a potential target against metabolic and age-related deterioration.","dates":{"publication":"2026/02/17"},"accession":"GSE174547","cross_references":{"GSM":["GSM5319407","GSM5319406","GSM5319405","GSM5319404","GSM5319403","GSM5319402","GSM5319401","GSM5319400","GSM5319399"],"GPL":["17021"],"SRA":["SRP320114"],"GSE":["174547"],"taxon":["Mus musculus"]}}