Evidence map›Paper›PMID 26568417›Full record

ArticleAging2015

Apoptosis during embryonic tissue remodeling is accompanied by cell senescence.

Carlos I Lorda-Diez, Beatriz Garcia-Riart, Juan A Montero, Joaquín Rodriguez-León, Juan A Garcia-Porrero, Juan M Hurle

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

37 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Adaptive evolution ofZoological research · 2025
    Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Cellular senescence in brain aging and cognitive decline.Frontiers in aging neuroscience · 2023
    Review
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review
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

6 authors at 2 institutions in 1 country.

Carlos I Lorda-DiezDepartamento de Anatomía y Biología Celular and IDIVAL, Universidad de Cantabria, Santander 39011, Spain.
Beatriz Garcia-RiartDepartamento de Anatomía y Biología Celular and IDIVAL, Universidad de Cantabria, Santander 39011, Spain.
Juan A MonteroDepartamento de Anatomía y Biología Celular and IDIVAL, Universidad de Cantabria, Santander 39011, Spain.
Joaquín Rodriguez-LeónDepartamento de Anatomía y Biología Celular,Universidad de Extremadura, Badajoz 07006, Spain.
Juan A Garcia-PorreroDepartamento de Anatomía y Biología Celular and IDIVAL, Universidad de Cantabria, Santander 39011, Spain.
Juan M HurleDepartamento de Anatomía y Biología Celular and IDIVAL, Universidad de Cantabria, Santander 39011, Spain.
Universidad de Cantabria · ESUniversidad de Extremadura · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study re-examined the dying process in the interdigital tissue during the formation of free digits in the developing limbs. We demonstrated that the interdigital dying process was associated with cell senescence, as deduced by induction of β-gal activity, mitotic arrest, and transcriptional up-regulation of p21 together with many components of the senescence-associated secretory phenotype. We also found overlapping domains of expression of members of the Btg/Tob gene family of antiproliferative factors in the regressing interdigits. Notably, Btg2 was up-regulated during interdigit remodeling in species with free digits but not in the webbed foot of the duck. We also demonstrate that oxidative stress promoted the expression of Btg2, and that FGF2 and IGF1 which are survival signals for embryonic limb mesenchyme inhibited Btg2 expression. Btg2 overexpression in vivo and in vitro induced all the observed changes during interdigit regression, including oxidative stress, arrest of cell cycle progression, transcriptional regulation of senescence markers, and caspase-mediated apoptosis. Consistent with the central role of p21 on cell senescence, the transcriptional effects induced by overexpression of Btg2 are attenuated by silencing p21. Our findings indicate that cell senescence and apoptosis are complementary processes in the regression of embryonic tissues and share common regulatory signals.

Indexed as

ApoptosisCellular SenescenceAnimalsChick EmbryoExtremitiesHumansImmediate-Early ProteinsIntracellular Signaling Peptides and ProteinsMesodermMiceMice, Inbred C57BLOxidative StressTumor Suppressor ProteinsBTG2 protein, humanImmediate-Early ProteinsIntracellular Signaling Peptides and ProteinsTOB1 protein, humanTumor Suppressor ProteinsINZlimb developmentprogrammed cell deathSASPsenescencesyndactylyβ-galactosidase

Identifiers

PMID26568417
PMCPMC4694067
OpenAlexW2334260316

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.