Evidence map›Paper›PMID 35993337›Full record

ArticleeLife2022

A regeneration-triggered metabolic adaptation is necessary for cell identity transitions and cell cycle re-entry to support blastema formation and bone regeneration.

Ana S Brandão, Jorge Borbinha, Telmo Pereira, Patrícia H Brito, Raquel Lourenço, Anabela Bensimon-Brito, Antonio Jacinto

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.5field-weighted citation impact, top 6% of its field
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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Signal control during tissue regeneration in adult animals.Nature reviews. Molecular cell biology · 2026
    Review
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  15. Review
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  17. Metabolic switches during development and regeneration.Development (Cambridge, England) · 2023
    Review
  18. Review
  19. Article
  20. Aerobic glycolysis is important for zebrafish larval wound closure and tail regeneration.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2022
    Article
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

7 authors at 2 institutions in 2 countries.

Ana S BrandãoCEDOC, NOVA Medical School, Universidade Nova de Lisboa, Lisbon, Portugal.ORCID 0000-0001-5842-033X
Jorge BorbinhaCEDOC, NOVA Medical School, Universidade Nova de Lisboa, Lisbon, Portugal.ORCID 0000-0003-0720-5642
Telmo PereiraCEDOC, NOVA Medical School, Universidade Nova de Lisboa, Lisbon, Portugal.ORCID 0000-0002-6903-9187
Patrícia H BritoUCIBIO, Dept. Ciências da Vida, Faculdade de Ciências e Tecnologia, Universidade NOVA de Lisboa, Lisbon, Portugal.
Raquel LourençoCEDOC, NOVA Medical School, Universidade Nova de Lisboa, Lisbon, Portugal.ORCID 0000-0002-6176-3066
Anabela Bensimon-BritoINSERM, ATIP-Avenir, Aix Marseille Univ, Marseille Medical Genetics, Marseille, France.
Antonio JacintoCEDOC, NOVA Medical School, Universidade Nova de Lisboa, Lisbon, Portugal.ORCID 0000-0002-4193-6089
Universidade Nova de Lisboa · PTInserm · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regeneration depends on the ability of mature cells at the injury site to respond to injury, generating tissue-specific progenitors that incorporate the blastema and proliferate to reconstitute the original organ architecture. The metabolic microenvironment has been tightly connected to cell function and identity during development and tumorigenesis. Yet, the link between metabolism and cell identity at the mechanistic level in a regenerative context remains unclear. The adult zebrafish caudal fin, and bone cells specifically, have been crucial for the understanding of mature cell contribution to tissue regeneration. Here, we use this model to explore the relevance of glucose metabolism for the cell fate transitions preceding new osteoblast formation and blastema assembly. We show that injury triggers a modulation in the metabolic profile at early stages of regeneration to enhance glycolysis at the expense of mitochondrial oxidation. This metabolic adaptation mediates transcriptional changes that make mature osteoblast amenable to be reprogramed into pre-osteoblasts and induces cell cycle re-entry and progression. Manipulation of the metabolic profile led to severe reduction of the pre-osteoblast pool, diminishing their capacity to generate new osteoblasts, and to a complete abrogation of blastema formation. Overall, our data indicate that metabolic alterations have a powerful instructive role in regulating genetic programs that dictate fate decisions and stimulate proliferation, thereby providing a deeper understanding on the mechanisms regulating blastema formation and bone regeneration.

Indexed as

Animal FinsZebrafishAnimalsBone RegenerationCell DivisionZebrafish ProteinsZebrafish Proteinsblastemacell fatecell metabolismdedifferentiationosteoblastregenerationregenerative medicinestem cellszebrafish

Identifiers

PMID35993337
PMCPMC9395193
OpenAlexW4291552268

What OpenQuestion holds

Textmetadata
LicenceCC BY
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 OpenQuestion graph.