Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation

Zhou S., Wang L., Chen N., Liu J., Zhang R., Zhou S.

Narrative Review on Chronic Wound, Scar, Chronic Inflammation, published in Front Immunol (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Front Immunol (2026)
Reported sample size
—
Source database
Europe PMC
PMID
42112383
PMCID
PMC13152729
DOI
10.3389/fimmu.2026.1792028

Abstract (original English)

Keloids are chronic inflammatory fibroproliferative disorders characterized by invasive growth beyond the original wound margins and a high recurrence rate, substantially impairing patients' quality of life. Their pathogenesis is complex and arises from the synergistic interplay among the mechanical microenvironment, chronic inflammation, and profibrotic signaling networks. The inflammatory and proliferative phases of normal wound healing are pathologically prolonged, with sustained activation of fibroblasts and myofibroblasts, resulting in excessive extracellular matrix (ECM) deposition and aberrant remodeling. Within the immune microenvironment, infiltrating M2 macrophages and Th2/Th17 cells, among others, secrete a broad array of cytokines, thereby establishing a chronic inflammatory circuit. Mechanical forces act as a pivotal driving factor: stress concentration in high-tension regions and activation of fibroblast mechanotransduction pathways (e.g., Hippo-YAP/TAZ and integrin-FAK) interact with inflammatory responses to form a self-amplifying "mechanical force-inflammation-fibrosis" positive feedback loop, exacerbating disease progression. Current management primarily relies on multimodal regimens such as surgery combined with radiotherapy and intralesional pharmacologic injections, yet remains challenged by high recurrence rates and marked heterogeneity. In recent years, t

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
AnimalsHumansKeloidInflammationCytokinesMechanotransduction, CellularStress, Mechanical

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