ArticleScientific reports2019
Sirtuin 3 deficiency does not impede digit regeneration in mice.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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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
10 citing papers in PubMed.
- Osteoprogenitor cells from non-regenerative bone show greater resistance to cellular stress than those from regenerative bone.Frontiers in cell and developmental biology · 2025Article
- M2 macrophages secrete glutamate-containing extracellular vesicles to alleviate osteoporosis by reshaping osteoclast precursor fate.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Targeting Glycolytic Reprogramming in Cholangiocarcinoma: A Novel Approach for Metabolic Therapy.Journal of inflammation research · 2024Review
- Oxaloacetate enhances and accelerates regeneration in young mice by promoting proliferation and mineralization.Frontiers in cell and developmental biology · 2023Article
- Evaluating differences in Young's Modulus of regenerated and uninjured mouse digit bone through microCT density-based calculation and nanoindentation testing.Journal of biomechanics · 2022Article
- Spatial transcriptomics reveals metabolic changes underly age-dependent declines in digit regeneration.eLife · 2022Article
- Epimorphic regeneration of the mouse digit tip is finite.Stem cell research & therapy · 2022Article
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency.JCI insight · 2021Article
- Article
- Age-Dependent Changes in Bone Architecture, Patterning, and Biomechanics During Skeletal Regeneration.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
The mitochondrial deacetylase sirtuin 3 (SIRT3) is thought to be one of the main contributors to metabolic flexibility-promoting mitochondrial energy production and maintaining homeostasis. In bone, metabolic profiles are tightly regulated and the loss of SIRT3 has deleterious effects on bone volume in vivo and on osteoblast differentiation in vitro. Despite the prominent role of this protein in bone stem cell proliferation, metabolic activity, and differentiation, the importance of SIRT3 for regeneration after bone injury has never been reported. We show here, using the mouse digit amputation model, that SIRT3 deficiency has no impact on the regenerative capacity and architecture of bone and soft tissue. Regeneration occurs in SIRT3 deficient mice in spite of the reduced oxidative metabolic profile of the periosteal cells. These data suggest that bone regeneration, in contrast to homeostatic bone turnover, is not reliant upon active SIRT3, and our results highlight the need to examine known roles of SIRT3 in the context of injury.
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Registered trials
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.