The DOI matches its Crossref record; 80 of the 81 references it cites were found in a registry or an index.
Mitochondrial dynamics maintain muscle stem cell regenerative competence throughout adult life by regulating metabolism and mitophagy
Open accessAbstract
Skeletal muscle regeneration depends on the correct expansion of resident quiescent stem cells (satellite cells), a process that becomes less efficient with aging. Here, we show that mitochondrial dynamics are essential for the successful regenerative capacity of satellite cells. The loss of mitochondrial fission in satellite cells-due to aging or genetic impairment-deregulates the mitochondrial electron transport chain (ETC), leading to inefficient oxidative phosphorylation (OXPHOS) metabolism and mitophagy and increased oxidative stress. This state results in muscle regenerative failure, which is caused by the reduced proliferation and functional loss of satellite cells. Regenerative functions can be restored in fission-impaired or aged satellite cells by the re-establishment of mitochondrial dynamics (by activating fission or preventing fusion), OXPHOS, or mitophagy. Thus, mitochondrial shape and physical networking controls stem cell regenerative functions by regulating metabolism and proteostasis. As mitochondrial fission occurs less frequently in the satellite cells in older humans, our findings have implications for regeneration therapies in sarcopenia.
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“During ageing, tissue regenerative functions decline, in part due to stem cell-intrinsic accumulation of damage (for example, DNA damage, loss of proteostasis and oxidative damage), functional decay of niche cells and increased inflammation (inflammageing)4–9 through uncharacterized mechanisms.”
From Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration (2023) · cites this paper as [9]
In the citing paper
“This process is essential for regulating muscle stem cell regeneration by regulating metabolism, protein balance, and mitophagy for regenerative therapies in sarcopenia [56].”
From Exerkines and Sarcopenia: Unveiling the Mechanism Behind Exercise-Induced Mitochondrial Homeostasis (2025) · cites this paper as [56]
Citations
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1 of the 81 references couldn’t be matched to a known paper.
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Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances
Xu, X., Pang, Y., & Fan, X. (2025) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-025-02253-4 · Cited by 1,016
Mitophagy in human health, ageing and disease
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“This indicates that the age-related decrease in satellite cell regenerative capacity can be partly ascribed to reduced mitochondrial signalling control 43 .”
Multifaceted mitochondria: moving mitochondrial science beyond function and dysfunction
Monzel, A. S., Enrı́quez, J. A., & Picard, M. A. (2023) · Nature Metabolism · doi:10.1038/s42255-023-00783-1 · Cited by 632
Senescence atlas reveals an aged-like inflamed niche that blunts muscle regeneration
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Sarcopenic obesity: Emerging mechanisms and therapeutic potential
Axelrod, C. L., Dantas, W. S., & Kirwan, J. P. (2023) · Metabolism · doi:10.1016/j.metabol.2023.155639 · Cited by 204
“Consistently, restoration of oxidative phosphorylation (OXPHOS) capacity and mitochondrial quality control rescues the regenerative failure of excessive mitochondrial fission in aged satellite cells [43].”
Background
Metadata
- Authors
- Hong, X., Isern, J., Campanario, S., Perdiguero, E., Ramírez-Pardo, I., Segalés, J., Hernansanz-Agustín, P., Curtabbi, A., Deryagin, O., Pollán, A., González-Reyes, J. A., Villalba, J. M., Sandri, M., Serrano, A. L., Enríquez, J. A., & Muñoz-Cánoves, P.
- Affiliations
- Spanish National Centre for Cardiovascular Research (ES)
- Universitat Pompeu Fabra (ES)
- University of Córdoba (ES)
- University of Padua (IT)
- ORCID
- Venue
- Cell stem cell
- Publisher
- Elsevier BV
- Published
- 2022-09
- Volume
- 29
- Issue
- 9
- Pages
- 1298-1314.e10
- ISSN
- 1875-9777 (ISSN-L)
- 1934-5909
- OpenAlex
- W4292646798
- Cited by
- 213
- References
- 81
- Citations by year
- 2026: 53 · 2025: 68 · 2024: 51 · 2023: 36 · 2022: 5
- FWCI
- 13.05
- Type
- journal article
- Language
- en
- Update notices
- erratum (2022-10-06)
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cell stem cell (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Repositori digital de la UPF (Universitat Pompeu Fabra) (submittedVersion, cc-by-nc-nd)
- Padua Research Archive (University of Padova) (submittedVersion)
- Funders
- Centro de Investigación Biomédica en Red Fragilidad y Envejecimiento Saludable (CIBERFES16/10/00282)
- Milky Way Research Foundation
- European Commission (H2020, 202033, 825825)
- Associazione Italiana per la Ricerca sul Cancro
- Centro Nacional de Investigaciones Cardiovasculares (MDM-2014-0370, SEV‐2015‐0505, HR17-00040, ERC-2016-AdG-741966, UPGRADE-H2020-825825)
- Horizon 2020 Framework Programme (UPGRADE-H2020-825825, 825825)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- mitochondrial dynamics, satellite cells, muscle regeneration, aging, mitochondrial fission, mitochondrial fusion, mitophagy, oxidative phosphorylation, electron transport chain, oxidative stress, stem cell quiescence, sarcopenia, skeletal muscle stem cells
- MeSH terms
- Aged, Humans, Mitochondria, Muscles, Stem Cells, Muscle, Skeletal, Mitochondrial Dynamics, Mitophagy
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