{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Costa-Machado LF"],"funding":["Austrian Science Fund FWF","ZonMw","Ministerio de Educación, Cultura y Deporte","Fundación Científica Asociación Española Contra el Cáncer","Generalitat Valenciana","NIH HHS"],"pagination":["2779"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC10185515"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["14(1)"],"pubmed_abstract":["Reversible and sub-lethal stresses to the mitochondria elicit a program of compensatory responses that ultimately improve mitochondrial function, a conserved anti-aging mechanism termed mitohormesis. Here, we show that harmol, a member of the beta-carbolines family with anti-depressant properties, improves mitochondrial function and metabolic parameters, and extends healthspan. Treatment with harmol induces a transient mitochondrial depolarization, a strong mitophagy response, and the AMPK compensatory pathway both in cultured C2C12 myotubes and in male mouse liver, brown adipose tissue and muscle, even though harmol crosses poorly the blood-brain barrier. Mechanistically, simultaneous modulation of the targets of harmol monoamine-oxidase B and GABA-A receptor reproduces harmol-induced mit"],"journal":["Nature communications"],"pubmed_title":["Peripheral modulation of antidepressant targets MAO-B and GABAAR by harmol induces mitohormesis and delays aging in preclinical models."],"pmcid":["PMC10185515"],"funding_grant_id":["W 1226","MGS/2021/15","CIDENGENT/2019/044","P40 OD010440","91715305","LABAE18008FERN","P 27893","P 29203","P 31727","OP ERDF","TAI 602","P 33957","P 29262"],"pubmed_authors":["Plaza A","Eisenberg T","Gomez-Cabrera MC","Duerr JS","Vina J","Costa-Machado LF","Hofer SJ","Loza MI","Villanueva-Bermejo D","Magnes C","Perez M","Del Pino I","Pozo OJ","Garcia-Dominguez E","Fornari T","Herradon G","Lopez-Aceituno JL","McIntyre RL","Gomez J","Tapia-Gonzalez A","Sierra-Ramirez A","Fernandez-Marcos PJ","Fabregat-Safont D","Madeo F","Ballesteros-Gonzalez A","Galindo MI","Megias D","Houtkooper RH"],"additional_accession":[]},"is_claimable":false,"name":"Peripheral modulation of antidepressant targets MAO-B and GABAAR by harmol induces mitohormesis and delays aging in preclinical models.","description":"Reversible and sub-lethal stresses to the mitochondria elicit a program of compensatory responses that ultimately improve mitochondrial function, a conserved anti-aging mechanism termed mitohormesis. Here, we show that harmol, a member of the beta-carbolines family with anti-depressant properties, improves mitochondrial function and metabolic parameters, and extends healthspan. Treatment with harmol induces a transient mitochondrial depolarization, a strong mitophagy response, and the AMPK compensatory pathway both in cultured C2C12 myotubes and in male mouse liver, brown adipose tissue and muscle, even though harmol crosses poorly the blood-brain barrier. Mechanistically, simultaneous modulation of the targets of harmol monoamine-oxidase B and GABA-A receptor reproduces harmol-induced mit","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 May","modification":"2026-05-29T13:00:53.485Z","creation":"2025-02-19T04:44:15.232Z"},"accession":"S-EPMC10185515","cross_references":{"pubmed":["37188705"],"doi":["10.1038/s41467-023-38410-y"]}}