ArticleNature communications2023
Peripheral modulation of antidepressant targets MAO-B and GABAAR by harmol induces mitohormesis and delays aging in preclinical models.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Spermidine Mitigates Immune Cell Senescence and Boosts Vaccine Responses in Healthy Older Adults-A Pilot Study.Aging cell · 2026Trial
- Exercise and dietary interventions in the regulation of hepatic mitophagy and liver recovery (Review).Biomedical reports · 2026Review
- Molecules of mood: the integrated molecular transducers of exercise's antidepressant effects.Molecular genetics and genomics : MGG · 2026Review
- Reserpine prolongs lifespan but compromises locomotion and heat-stress resilience in Drosophila melanogaster.npj aging · 2026Article
- Leveraging mitochondrial stress to improve healthy aging.Sports medicine and health science · 2026Review
- Gut microbiota phospholipids regulate intestinal gene expression and can counteract the effects of antibiotic treatment.Research square · 2025Article
- The MAO-B Inhibitor Selegiline Reduces the Viability of Different Prostate Cancer Cell Lines and Enhances the Effects of Anti-Androgen and Cytostatic Agents.Pharmacology research & perspectives · 2025Article
- Mammalian mitohormesis: from mitochondrial stressors to organismal benefits.The EMBO journal · 2025Review
- Spermidine supplementation and protein restriction protect from organismal and brain aging independently.Aging · 2025Article
- Targeting GABA signaling in type 1 diabetes and its complications- an update on the state of the art.Pharmacological reports : PR · 2025Review
- Efficacy and mechanism of action of harmine derivative H-2-104 against Echinococcus granulosus infection in mice.BMC veterinary research · 2025Article
- Exertional Exhaustion (Post-Exertional Malaise, PEM) Evaluated by the Effects of Exercise on Cerebrospinal Fluid Metabolomics-Lipidomics and Serine Pathway in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome.International journal of molecular sciences · 2025Article
- Unveiling the Longevity Potential of Natural Phytochemicals: A Comprehensive Review of Active Ingredients in Dietary Plants and Herbs.Journal of agricultural and food chemistry · 2024Review
- Spermidine is essential for fasting-mediated autophagy and longevity.Nature cell biology · 2024Article
- Stanniocalcin 2 governs cancer cell adaptation to nutrient insufficiency through alleviation of oxidative stress.Cell death & disease · 2024Article
- Formation, Identification, and Occurrence of the Furan-Containing β-Carboline Flazin Derived from l-Tryptophan and Carbohydrates.Journal of agricultural and food chemistry · 2024Article
- Stanniocalcin 2 governs cancer cell adaptation to nutrient insufficiency through alleviation of oxidative stress.Research square · 2024Article
- The missing hallmark of health: psychosocial adaptation.Cell stress · 2024Article
- Mitohormesis.Cell metabolism · 2023Review
- Article
Corrections and comments
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Authors and funding
28 authors at 14 institutions in 4 countries.
Funding
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 mitochondrial improvements. Diet-induced pre-diabetic male mice improve their glucose tolerance, liver steatosis and insulin sensitivity after treatment with harmol. Harmol or a combination of monoamine oxidase B and GABA-A receptor modulators extend the lifespan of hermaphrodite Caenorhabditis elegans or female Drosophila melanogaster. Finally, two-year-old male and female mice treated with harmol exhibit delayed frailty onset with improved glycemia, exercise performance and strength. Our results reveal that peripheral targeting of monoamine oxidase B and GABA-A receptor, common antidepressant targets, extends healthspan through mitohormesis.
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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.