Evidence map›Paper›PMID 38579709›Full record

ArticleStem cell reports2024

PINK1 deficiency alters muscle stem cell fate decision and muscle regenerative capacity.

George Cairns, Madhavee Thumiah-Mootoo, Mah Rukh Abbasi, Melissa Gourlay, Jeremy Racine, Nikita Larionov, Alexandre Prola, Mireille Khacho, Yan Burelle

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed.

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  2. Mitochondrial CaAntioxidants (Basel, Switzerland) · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

George CairnsInterdisciplinary School of Health Sciences, Faculty of Health Sciences, University of Ottawa, Ottawa, ON, Canada.
Madhavee Thumiah-MootooDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Mah Rukh AbbasiDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Melissa GourlayDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Jeremy RacineDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Nikita LarionovDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada.
Alexandre ProlaDepartment of Cell Physiology and Metabolism, University of Geneva, Switzerland.
Mireille KhachoDepartment of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada; Ottawa Institute of Systems Biology (OISB), Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada; Center for Neuromuscular Disease (CNMD), Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada.
Yan BurelleInterdisciplinary School of Health Sciences, Faculty of Health Sciences, University of Ottawa, Ottawa, ON, Canada; Department of Biochemistry, Microbiology and Immunology, University of Ottawa, Ottawa, ON, Canada. Electronic address: yburell2@uottawa.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintenance of mitochondrial function plays a crucial role in the regulation of muscle stem cell (MuSC), but the underlying mechanisms remain ill defined. In this study, we monitored mitophagy in MuSCS under various myogenic states and examined the role of PINK1 in maintaining regenerative capacity. Results indicate that quiescent MuSCs actively express mitophagy genes and exhibit a measurable mitophagy flux and prominent mitochondrial localization to autophagolysosomes, which become rapidly decreased during activation. Genetic disruption of Pink1 in mice reduces PARKIN recruitment to mitochondria and mitophagy in quiescent MuSCs, which is accompanied by premature activation/commitment at the expense of self-renewal and progressive loss of muscle regeneration, but unhindered proliferation and differentiation capacity. Results also show that impaired fate decisions in PINK1-deficient MuSCs can be restored by scavenging excess mitochondrial ROS. These data shed light on the regulation of mitophagy in MuSCs and position PINK1 as an important regulator of their mitochondrial properties and fate decisions.

Indexed as

Cell DifferentiationMitophagyProtein KinasesRegenerationStem CellsAnimalsCell ProliferationMiceMitochondriaMuscle DevelopmentMuscle, SkeletalReactive Oxygen SpeciesUbiquitin-Protein LigasesProtein KinasesReactive Oxygen SpeciesUbiquitin-Protein Ligasesfate decisionmitochondriamitochondrial quality controlmitophagymuscle regenerationmuscle stem cells

Identifiers

PMID38579709
PMCPMC11103785

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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 Socratic graph.