Evidence map›Paper›PMID 33042026›Full record

ReviewFrontiers in endocrinology2020

Cellular Senescence as the Pathogenic Hub of Diabetes-Related Wound Chronicity.

Jorge A Berlanga-Acosta, Gerardo E Guillén-Nieto, Nadia Rodríguez-Rodríguez, Yssel Mendoza-Mari, Maria Luisa Bringas-Vega, Jorge O Berlanga-Saez, Diana García Del Barco Herrera, Indira Martinez-Jimenez, Sandra Hernandez-Gutierrez, Pedro A Valdés-Sosa

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
6.1field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 102 citations in OpenAlex.

  1. Article
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  6. Article
  7. Article
  8. Article
  9. Portable Bioprinter in Ischemic Wound Therapy: a Pilot Study.Sovremennye tekhnologii v meditsine · 2026
    Article
  10. Article
  11. Review
  12. A synergistic multimodality treatment approach to address the key drivers of wound chronicity.Journal of vascular surgery. Venous and lymphatic disorders · 2026
    Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Article
  20. Review

4 more citing papers are in PubMed but not listed here.

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

10 authors at 4 institutions in 3 countries.

Jorge A Berlanga-AcostaThe Clinical Hospital Chengdu Brain Sciences Institute, University of Electronic Science and Technology of China, Chengdu, China.
Gerardo E Guillén-NietoThe Clinical Hospital Chengdu Brain Sciences Institute, University of Electronic Science and Technology of China, Chengdu, China.
Nadia Rodríguez-RodríguezTissue Repair, Wound Healing and Cytoprotection Research Group, Biomedical Research Direction, Center for Genetic Engineering and Biotechnology, Playa, Cuba.
Yssel Mendoza-MariTissue Repair, Wound Healing and Cytoprotection Research Group, Biomedical Research Direction, Center for Genetic Engineering and Biotechnology, Playa, Cuba.
Maria Luisa Bringas-VegaThe Clinical Hospital Chengdu Brain Sciences Institute, University of Electronic Science and Technology of China, Chengdu, China.
Jorge O Berlanga-SaezApplied Mathematics Department, Institute of Mathematics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Diana García Del Barco HerreraTissue Repair, Wound Healing and Cytoprotection Research Group, Biomedical Research Direction, Center for Genetic Engineering and Biotechnology, Playa, Cuba.
Indira Martinez-JimenezTissue Repair, Wound Healing and Cytoprotection Research Group, Biomedical Research Direction, Center for Genetic Engineering and Biotechnology, Playa, Cuba.
Sandra Hernandez-GutierrezDepartment of Surgery, Hospital Salvador Allende, Havana, Cuba.
Pedro A Valdés-SosaThe Clinical Hospital Chengdu Brain Sciences Institute, University of Electronic Science and Technology of China, Chengdu, China.
Centro de Ingeniería Genética y Biotecnología · CUCuban Neuroscience Center · CUUniversidade Federal do Rio de Janeiro · BRUniversity of Electronic Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetes is constantly increasing at a rate that outpaces genetic variation and approaches to pandemic magnitude. Skin cells physiology and the cutaneous healing response are progressively undermined in diabetes which predisposes to lower limb ulceration, recidivism, and subsequent lower extremities amputation as a frightened complication. The molecular operators whereby diabetes reduces tissues resilience and hampers the repair mechanisms remain elusive. We have accrued the notion that diabetic environment embraces preconditioning factors that definitively propel premature cellular senescence, and that ulcer cells senescence impair the healing response. Hyperglycemia/oxidative stress/mitochondrial and DNA damage may act as major drivers sculpturing the senescent phenotype. We review here historical and recent evidences that substantiate the hypothesis that diabetic foot ulcers healing trajectory, is definitively impinged by a self-expanding and self-perpetuative senescent cells society that drives wound chronicity. This society may be fostered by a diabetic archetypal secretome that induces replicative senescence in dermal fibroblasts, endothelial cells, and keratinocytes. Mesenchymal stem cells are also susceptible to major diabetic senescence drivers, which accounts for the inability of these cells to appropriately assist in diabetics wound healing. Thus, the use of autologous stem cells has not translated in significant clinical outcomes. Novel and multifaceted therapeutic approaches are required to pharmacologically mitigate the diabetic cellular senescence operators and reduce the secondary multi-organs complications. The senescent cells society and its adjunctive secretome could be an ideal local target to manipulate diabetic ulcers and prevent wound chronification and acute recidivism. This futuristic goal demands harnessing the diabetic wound chronicity epigenomic signature.

Indexed as

Cellular SenescenceDiabetic FootDNA DamageHumansMesenchymal Stem CellsOxidative StressWound Healingagingchronic woundsdiabetic ulcersproliferative senescencesenescence

Identifiers

PMID33042026
PMCPMC7525211
OpenAlexW3086808603

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.