Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (713 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
A sharply elevated, irregularly shaped, progressively enlarging scar resulting from formation of excessive amounts of collagen in the dermis during connective tissue repair. It is differentiated from a hypertrophic scar (cicatrix, hypertrophic) in that the former does not spread to surrounding tissues.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Keloids.
Where it fits in the MeSH classification
- Broader topics
- Cicatrix; Collagen Diseases
- Narrower topics
- Acne Keloid
- See also
- Cicatrix, Hypertrophic
Related concepts
- Cicatrix
- Hypertrophic
Research landscape
PubMed indexes 4,924 records tagged with the MeSH heading “Keloid” (counts retrieved 2026-10-31). 1,297 of them (26.3%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,464 records.
Reviews account for 642 records (13.0%) and meta-analyses for 57. Randomized controlled trials number 126 (2.6%) as a share of all records on the topic.
Show the data
| Period | Records |
|---|---|
| through 1999 | 1,464 |
| 2000-2009 | 869 |
| 2010-2019 | 1,294 |
| 2020 onward | 1,297 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 642 | 13.0% |
| Meta-analyses | 57 | 1.2% |
| Randomized controlled trials | 126 | 2.6% |
Method: PubMed query "Keloid"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-31.
Reading the evidence in anatomy and physiology
Anatomy describes how body structures are built and physiology describes how they normally work, so most findings here are descriptive or mechanistic rather than evidence about treatment. Much of what is known comes from dissection, imaging, tissue studies and experiments in animals, and measurements in healthy volunteers can differ from those in people with disease or at different ages. Normal ranges vary between individuals and populations. Check whether a result was measured in people or in another species, the age and health of the participants, and the method used.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| The Roles of Inflammation in Keloid and Hypertrophic Scars | 2020 | Review article Design not recorded in structured metadata | 301 | cc by PMID 33343575 · DOI · PMC7746641 |
| Keloid treatments: an evidence-based systematic review of recent advances | 2023 | Systematic review Design not recorded in structured metadata | 106 | cc by PMID 36918908 · DOI · PMC10012475 |
| RNA Sequencing Keloid Transcriptome Associates Keloids With Th2, Th1, Th17/Th22, and JAK3-Skewing | 2020 | Research article Design not recorded in structured metadata | 88 | cc by PMID 33329590 · DOI · PMC7719808 |
| Exploring the Complexities of TGF-β Signaling in Keloids: Beyond the Classical Smad Pathway | 2026 | Review article Design not recorded in structured metadata | 3 | cc by PMID 42074238 · DOI · PMC13116467 |
The Roles of Inflammation in Keloid and Hypertrophic Scars [1]
Abstract reading summary — source excerpts
- Opening excerpt
- The underlying mechanisms of wound healing are complex but inflammation is one of the determining factors.
- Closing excerpt
- Understanding the initiation, progression, and resolution of inflammation will provide insights into the mechanisms of scar formation and is useful for developing effective treatments.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (151 words)
The underlying mechanisms of wound healing are complex but inflammation is one of the determining factors. Besides its traditional role in combating against infection upon injury, the characteristics and magnitude of inflammation have dramatic impacts on the pathogenesis of scar. Keloids and hypertrophic scars are pathological scars that result from aberrant wound healing. They are characterized by continuous local inflammation and excessive collagen deposition. In this review, we aim at discussing how dysregulated inflammation contributes to the pathogenesis of scar formation. Immune cells, soluble inflammatory mediators, and the related intracellular signal transduction pathways are our three subtopics encompassing the events occurring in inflammation associated with scar formation. In the end, we enumerate the current and potential medicines and therapeutics for suppressing inflammation and limiting progression to scar. Understanding the initiation, progression, and resolution of inflammation will provide insights into the mechanisms of scar formation and is useful for developing effective treatments.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33343575 · DOI · PMC7746641
Keloid treatments: an evidence-based systematic review of recent advances [2]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundKeloids are pathologic scars that pose a significant functional and cosmetic burden.
- Closing excerpt
- Larger and more robust controlled studies are necessary to further understand the variety of existing and emerging keloid treatments, including corticosteroids, cryotherapy, intralesional injections, lasers, photodynamic therapy, excision and radiation, pressure dressings, and others.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (260 words)
BackgroundKeloids are pathologic scars that pose a significant functional and cosmetic burden. They are challenging to treat, despite the multitude of treatment modalities currently available.ObjectiveThe aim of this study was to conduct an evidence-based review of all prospective data regarding keloid treatments published between 2010 and 2020.MethodsA systematic literature search of PubMed (National Library of Medicine), Embase (Elsevier), and Cochrane Library (Wiley) was performed in November of 2020. Search strategies with the keywords "keloid" and "treatment" were performed by a medical librarian. The search was limited to prospective studies that were peer-reviewed, reported on clinical outcomes of keloid therapies, and were published in the English language between January 1, 2010, and November 24, 2020.ResultsA total of 3462 unique citations were identified, of which 108 studies met inclusion criteria. Current literature supports silicone gel or sheeting with corticosteroid injections as first-line therapy for keloids. Adjuvant intralesional 5-fluorouracil (5-FU), bleomycin, or verapamil can be considered, although mixed results have been reported with each. Laser therapy can be used in combination with intralesional corticosteroids or topical steroids with occlusion to improve drug penetration. Excision of keloids with immediate post-excision radiation therapy is an effective option for recalcitrant lesions. Finally, silicone sheeting and pressure therapy have evidence for reducing keloid recurrence.ConclusionsThis review was limited by heterogeneity of subject characteristics and study outcome measures, small sample sizes, and inconsistent study designs. Larger and more robust controlled studies are necessary to further understand the variety of existing and emerging keloid treatments, including corticosteroids, cryotherapy, intralesional injections, lasers, photodynamic therapy, excision and radiation, pressure dressings, and others.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36918908 · DOI · PMC10012475
RNA Sequencing Keloid Transcriptome Associates Keloids With Th2, Th1, Th17/Th22, and JAK3-Skewing [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Keloids are disfiguring, fibroproliferative growths and their pathogenesis remains unclear, inhibiting therapeutic development.
- Closing excerpt
- This advocates for the investigation of novel treatments targeting the Th2 axis and/or JAK/STAT-signaling in keloid patients.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (138 words)
Keloids are disfiguring, fibroproliferative growths and their pathogenesis remains unclear, inhibiting therapeutic development. Available treatment options have limited efficacy and harbor safety concerns. Thus, there is a great need to clarify keloid pathomechanisms that may lead to novel treatments. In this study, we aimed to elucidate the profile of lesional and non-lesional keloid skin compared to normal skin. We performed gene (RNAseq, qRT-PCR) and protein (immunohistochemistry) expression analyses on biopsy specimens obtained from lesional and non-lesional skin of African American (AA) keloid patients compared to healthy skin from AA controls. Fold-change≥2 and false-discovery rate (FDR)+, CCR9+, and periostin+ immunostaining. In sum, comprehensive molecular profiling demonstrated that both lesional and non-lesional skin show significant immune alternations, and particularly Th2 and JAK3 expression. This advocates for the investigation of novel treatments targeting the Th2 axis and/or JAK/STAT-signaling in keloid patients.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 33329590 · DOI · PMC7719808
Exploring the Complexities of TGF-β Signaling in Keloids: Beyond the Classical Smad Pathway [4]
Abstract reading summary — source excerpts
- Opening excerpt
- Keloid is a benign skin disease with excessive growth of fibroblasts, characterized by too much abnormal extracellular matrix deposited in the dermis.
- Closing excerpt
- Targeting these specific molecular hubs through combination and precision therapies serves to reprogram the fibrotic microenvironment.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (164 words)
Keloid is a benign skin disease with excessive growth of fibroblasts, characterized by too much abnormal extracellular matrix deposited in the dermis. It is generally believed that transforming growth factor-β (TGF-β) is the core cytokine that causes keloid. Previously, it was thought that its pathogenic effect was mainly attributed to the classical Smad-dependent pathway. It directly shuttles signals to the nucleus to trigger pro-fibrotic gene transcription. However, accumulating evidence now points to the equally vital role of Smad-independent signaling. Unlike the direct nuclear translocation of Smads, these alternative pathways transmit signals through rapid intracellular kinase cascades. They jointly direct the proliferation, migration, anti-apoptosis, fibrogenesis, and chronic inflammation of fibroblasts in keloids. This review attempts to comprehensively clarify the molecular processes regulated by TGF-β through non-Smad pathways (such as MAPK, PI3K/Akt, Rho GTPase, Wnt/β-catenin, JAK/STAT). Translating these non-Smad insights helps to overcome the high recurrence rates of traditional therapies. Targeting these specific molecular hubs through combination and precision therapies serves to reprogram the fibrotic microenvironment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 42074238 · DOI · PMC13116467
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Hypertrophic scarring and keloids: pathomechanisms and current and emerging treatment strategies [5]
- Research article Keloid and Hypertrophic Scars Are the Result of Chronic Inflammation in the Reticular Dermis [6]
- Research article International clinical recommendations on scar management [7]
- Research article On the nature of hypertrophic scars and keloids: a review [8]
- Research article Keloid pathogenesis and treatment [9]
- Research article Recent Understandings of Biology, Prophylaxis and Treatment Strategies for Hypertrophic Scars and Keloids [10]
References
- Wang ZC, Zhao WY, Cao Y, Liu YQ, Sun Q, Shi P, et al.. The Roles of Inflammation in Keloid and Hypertrophic Scars. . 2020. PMID 33343575 · DOI · PMC7746641
- Walsh LA, Wu E, Pontes D, Kwan KR, Poondru S, Miller CH, et al.. Keloid treatments: an evidence-based systematic review of recent advances. . 2023. PMID 36918908 · DOI · PMC10012475
- Wu J, Del Duca E, Espino M, Gontzes A, Cueto I, Zhang N, et al.. RNA Sequencing Keloid Transcriptome Associates Keloids With Th2, Th1, Th17/Th22, and JAK3-Skewing. . 2020. PMID 33329590 · DOI · PMC7719808
- Mo J, Huang H, Zhu B, Liao R, Li W, Zhang Y. Exploring the Complexities of TGF-β Signaling in Keloids: Beyond the Classical Smad Pathway. . 2026. PMID 42074238 · DOI · PMC13116467
- Gauglitz GG, Korting HC, Pavicic T, Ruzicka T, Jeschke MG. Hypertrophic scarring and keloids: pathomechanisms and current and emerging treatment strategies. Mol Med. 2011. PMID 20927486 · DOI · PMC3022978
- Ogawa R. Keloid and Hypertrophic Scars Are the Result of Chronic Inflammation in the Reticular Dermis. Int J Mol Sci. 2017. PMID 28287424 · DOI · PMC5372622
- Mustoe TA, Cooter RD, Gold MH, Hobbs FD, Ramelet AA, Shakespeare PG, et al.. International clinical recommendations on scar management. Plast Reconstr Surg. 2002. PMID 12142678 · DOI
- Niessen FB, Spauwen PH, Schalkwijk J, Kon M. On the nature of hypertrophic scars and keloids: a review. Plast Reconstr Surg. 1999. PMID 10513931 · DOI
- Al-Attar A, Mess S, Thomassen JM, Kauffman CL, Davison SP. Keloid pathogenesis and treatment. Plast Reconstr Surg. 2006. PMID 16404281 · DOI
- Lee HJ, Jang YJ. Recent Understandings of Biology, Prophylaxis and Treatment Strategies for Hypertrophic Scars and Keloids. Int J Mol Sci. 2018. PMID 29498630 · DOI · PMC5877572
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-10-31.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.