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Mitophagy in human health, ageing and disease
Open accessAbstract
Maintaining optimal mitochondrial function is a feature of health. Mitophagy removes and recycles damaged mitochondria and regulates the biogenesis of new, fully functional ones preserving healthy mitochondrial functions and activities. Preclinical and clinical studies have shown that impaired mitophagy negatively affects cellular health and contributes to age-related chronic diseases. Strategies to boost mitophagy have been successfully tested in model organisms, and, recently, some have been translated into clinics. In this Review, we describe the basic mechanisms of mitophagy and how mitophagy can be assessed in human blood, the immune system and tissues, including muscle, brain and liver. We outline mitophagy's role in specific diseases and describe mitophagy-activating approaches successfully tested in humans, including exercise and nutritional and pharmacological interventions. We describe how mitophagy is connected to other features of ageing through general mechanisms such as inflammation and oxidative stress and forecast how strengthening research on mitophagy and mitophagy interventions may strongly support human health.
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“Furthermore, ageing impairs the mitophagy process, reducing the clearance of damaged mitochondria and exacerbating cellular stress.190”
From Antiageing strategy for neurodegenerative diseases: from mechanisms to clinical advances (2025) · cites this paper as [190]
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Renal-targeted tFNA-TPP nanoagonist treats acute kidney injury by amplifying mitophagy
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Metadata
- Authors
- Picca, A., Faitg, J., Auwerx, J., Ferrucci, L., & D’Amico, D.
- Affiliations
- Agostino Gemelli University Polyclinic (IT)
- Amazentis (Switzerland) (CH)
- École Polytechnique Fédérale de Lausanne (CH)
- National Institute on Aging (US)
- Corresponding author
- Ferrucci, Luigi
- D’Amico, Davide
- Venue
- Nature Metabolism
- Published
- 2023-11-30
- Volume
- 5
- Issue
- 12
- Pages
- 2047-2061
- ISSN
- 2522-5812 (ISSN-L)
- PMC
- PMC12159423
- OpenAlex
- W4389166615
- Cited by
- 635
- References
- 190
- Citations by year
- 2026: 263 · 2025: 273 · 2024: 98 · 2023: 1
- FWCI
- 24.82
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- Locations
- Nature Metabolism (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
- Funders
- National Science Foundation
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (179435)
- National Institutes of Health (Z99 AG999999)
- H2020 European Research Council (787702)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Keywords
- mitophagy, mitochondrial function, mitochondrial biogenesis, aging, age-related chronic diseases, physical activity, dietary intervention, pharmacological interventions, inflammation, oxidative stress, immune system, muscle, brain, liver, blood biomarkers
- MeSH terms
- Aging, Humans, Mitochondria, Oxidative Stress, Mitophagy
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