Evidence mapPaperPMID 41479883Full record

ReviewFrontiers in immunology2025

Targeting persistently activated inflammatory microenvironment to promote chronic wound healing.

Yuxuan Dai, Yu Chen

Abstract readReview
In one paragraph

Review in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
field-weighted citation impact
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

12 citing papers in PubMed.

  1. Review
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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

2 authors.

Yuxuan DaiDepartment of Plastic Surgery, Beilun Branch of the First Affiliated Hospital, College of Medicine, Zhejiang University, Ningbo, Zhejiang, China.
Yu ChenDepartment of Surgical Oncology, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The immune system plays a pivotal role in maintaining the balance of inflammatory responses and facilitating tissue repair and wound healing. However, under the combined influence of immune microenvironmental factors and external stimuli, immune cell dysfunction can lead to persistent activation of the inflammatory milieu, resulting in delayed or impaired wound healing. Therefore, regulating immune responses within the chronic inflammatory microenvironment and suppressing aberrant immune cell activation not only helps restore immune homeostasis but also effectively accelerates the wound healing process. Identifying and modulating novel targets associated with macrophage and T-cell dysregulation, as well as the crosstalk among immune cells, offers new insights and therapeutic strategies for the treatment of chronic inflammation-related disorders and wound repair. This review focuses on the molecular mechanisms underlying aberrant macrophage and T-cell activation, the intercellular crosstalk within the immune microenvironment, and their impact on the wound healing process. Furthermore, it highlights potential therapeutic targets for limiting persistent inflammation and re-establishing immune homeostasis. Elucidating these mechanisms and targets may provide promising avenues for the treatment of chronic inflammatory diseases and for advancing strategies in tissue repair and regeneration.

Indexed as

Cellular MicroenvironmentInflammationWound HealingAnimalsChronic DiseaseHumansMacrophagesT-Lymphocytesdelayed healing woundsimmunoregulationinflammationmacrophagestissue repair

Identifiers

PMID41479883
PMCPMC12753479

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.