The SIRT1 activator SRT2104 exerts exercise mimetic effects and promotes Duchenne muscular dystrophy recovery
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Duchenne muscular dystrophy (DMD) is a devastating genetic disorder, whose management is still a major challenge, despite progress in genetic and pharmacological disease-modifying treatments have been made. Mitochondrial dysfunctions contribute to DMD, however, there are no effective mitochondrial therapies for DMD. SIRT1 is a NAD + -dependent deacetylase that controls several key processes and whose impairment is involved in determining mitochondrial dysfunction in DMD. In addition to well-known resveratrol, other potent selective activators of SIRT1 exist, with better pharmacokinetics properties and a safer profile. Among these, SRT2104 is the most promising and advanced in clinical studies. Here we unveil the beneficial effects of SRT2104 in flies, mice, and patient-derived myoblasts as different models of DMD, demonstrating an anti-inflammatory, anti-fibrotic, and pro-regenerative action of the drug. We elucidate, by molecular dynamics simulations, that a conformational selection mechanism is responsible for the activation of SIRT1. Further, the impact of SRT2104 in reshaping muscle proteome and acetylome profiles has been investigated, highlighting effects that mimic those induced by exercise. Overall, our data suggest SRT2104 as a possible therapeutic candidate to successfully counteract DMD progression.
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SRT2104 enhanced muscle function and regeneration and mitochondrial function, and promoted recovery in Duchenne muscular dystrophy models.
“Similarly, the sirtuin 1 activator, SRT2104, demonstrated to mimic the beneficial effects of exercise and enhance muscle function and regeneration, and mitochondrial function, thereby promoting recovery in Duchenne muscular dystrophy models [69].”
From Muscle loss and GLP-1R agonists use (2025) · cites this paper as [69]
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“Similarly, the sirtuin 1 activator, SRT2104, demonstrated to mimic the beneficial effects of exercise and enhance muscle function and regeneration, and mitochondrial function, thereby promoting recovery in Duchenne muscular dystrophy models [69].”
Self-citation
- Authors
- Giovarelli, M., Zecchini, S., Casati, S. R., Lociuro, L., Gjana, O., Mollica, L., Pisanu, E., Mbissam, H. D., Cappellari, O., De Santis, C., Arcari, A., Bigot, A., Clerici, G., Catalani, E., Del Quondam, S., Andolfo, A., Braccia, C., Cattaneo, M. G., Banfi, C., Brunetti, D., Mocciaro, E., De Luca, A., Clementi, E., Cervia, D., Perrotta, C., & De Palma, C.
- Affiliations
- University of Milan (IT)
- University of Bari Aldo Moro (IT)
- Inserm (FR)
- Human Technopole (IT)
- Università degli Studi della Tuscia (IT)
- IRCCS Ospedale San Raffaele (IT)
- Centro Cardiologico Monzino (IT)
- ORCID
- Venue
- Cell Death & Disease
- Published
- 2025-04-07
- Volume
- 16
- Issue
- 1
- Pages
- 259-259
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC11977210
- OpenAlex
- W4409214478
- Cited by
- 12
- References
- 82
- Citations by year
- 2026: 8 · 2025: 4
- FWCI
- 3.59
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death and Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Archivio Istituzionale della Ricerca (Universita Degli Studi Di Milano) (submittedVersion, other-oa)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UnitusOpen (Tuscia University) (submittedVersion)
- CINECA IRIS Institutional Research Information System (University of Bari Aldo Moro) (submittedVersion)
- Funders
- AFM-Téléthon (20568, 24077)
- Ministero della Salute (2017FJSM9S, 2020ELYA32004)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Geriatrics and Gerontology › Sirtuins and Resveratrol in Medicine
- Health Sciences › Medicine › Genetics › Neurogenetic and Muscular Disorders Research
- Keywords
- Duchenne muscular dystrophy, SRT2104, SIRT1 activators, mitochondrial dysfunction, exercise mimetics, muscle regeneration, anti-inflammatory activity, antifibrotic effect, conformational selection, NAD+-dependent deacetylase, muscle proteome, acetylome, resveratrol, disease-modifying therapy
- MeSH terms
- Animals, Disease Models, Animal, Humans, Male, Mice, Inbred C57BL, Mitochondria, Physical Conditioning, Animal, Mice, Inbred mdx, Muscle, Skeletal, Muscular Dystrophy, Duchenne, Myoblasts, Mice, Molecular Dynamics Simulation, Sirtuin 1
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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