Evidence map›Paper›PMID 38440347›Full record

ReviewFrontiers in physiology2024

Cellular senescence and wound healing in aged and diabetic skin.

Arisa Kita, Sena Yamamoto, Yuki Saito, Takako S Chikenji

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in physiology, 2024. 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
9.0field-weighted citation impact, top 2% 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, 36 citations in OpenAlex.

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  9. Quantifying Information Exchange Between Cells in Inflammaging.Bioengineering (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

4 authors at 3 institutions in 1 country.

Arisa KitaDepartment of Anatomy, Sapporo Medical University School of Medicine, Sapporo, Japan.
Sena YamamotoGraduate School of Health Sciences, Hokkaido University, Sapporo, Japan.
Yuki SaitoDepartment of Anatomy, Sapporo Medical University School of Medicine, Sapporo, Japan.
Takako S ChikenjiGraduate School of Health Sciences, Hokkaido University, Sapporo, Japan.
Sapporo Medical University · JPHokkaido University · JPSapporo University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cellular senescence is a biological mechanism that prevents abnormal cell proliferation during tissue repair, and it is often accompanied by the secretion of various factors, such as cytokines and chemokines, known as the senescence-associated secretory phenotype (SASP). SASP-mediated cell-to-cell communication promotes tissue repair, regeneration, and development. However, senescent cells can accumulate abnormally at injury sites, leading to excessive inflammation, tissue dysfunction, and intractable wounds. The effects of cellular senescence on skin wound healing can be both beneficial and detrimental, depending on the condition. Here, we reviewed the functional differences in cellular senescence that emerge during wound healing, chronic inflammation, and skin aging. We also review the latest mechanisms of wound healing in the epidermis, dermis, and subcutaneous fat, with a focus on cellular senescence, chronic inflammation, and tissue regeneration. Finally, we discuss the potential clinical applications of promoting and inhibiting cellular senescence to maximize benefits and minimize detrimental effects.

Indexed as

aged-skincellular senescencediabetic skinsenescence-associated secretory phenotypes (SASP)woundhealing

Identifiers

PMID38440347
PMCPMC10909996
OpenAlexW4391929350

What Socratic 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 Socratic graph.