ArticleCommunications biology2024
Single cell transcriptomics reveals the cellular heterogeneity of keloids and the mechanism of their aggressiveness.
Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
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.
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Who cites it
17 citing papers in PubMed.
- Integrated Transcriptomic Analysis Suggests a C1Q-Related Macrophage-Fibroblast Signaling Axis in Keloids.International journal of molecular sciences · 2026Article
- Cellular Senescence in Keloid Pathology: Mechanisms, Biomarkers, and Potential Therapeutic Targets.Biomedicines · 2026Review
- Single-cell transcriptomic profiling identifies YY1 as a key regulator of fibroblast plasticity in hypertrophic scar formation.Burns & trauma · 2026Article
- Spatiotemporal decoding of skin biology: development, aging, disease, and regeneration.Burns & trauma · 2026Article
- Mechanistic insights into Strontium-90 superficial radiotherapy in keloids: senescence-associated changes and ECM remodeling across cell-matrix scales.Frontiers in pharmacology · 2026Article
- Endothelial system dysregulation underlies keloid development and therapeutic targeting.Frontiers in cell and developmental biology · 2026Review
- Advances in the interplay between mechanical forces and inflammatory immunity in keloid formation.Frontiers in immunology · 2026Review
- Immune-dominated cellular heterogeneity and stromal plasticity in keloid infiltrating and hypercellular zones revealed by single-cell RNA sequencing.Frontiers in immunology · 2026Article
- Deciphering the cellular landscape of pathological scars.Burns & trauma · 2026Article
- Harnessing population genetics and animal models to uncover the genetics of skin scarring.Journal of plastic, reconstructive & aesthetic surgery : JPRAS · 2026Review
- Understanding and Advancing Wound Healing in the Era of Multi-Omic Technology.Bioengineering (Basel, Switzerland) · 2025Review
- Single‑cell RNA sequencing reveals fibroblast heterogeneity and identifies CLOCK as a key regulator in fibrotic skin diseases.Scientific reports · 2025Article
- Pirfenidone in Skin Fibrosis and Scarring: From Bench Insights to Clinical Data.Medical sciences (Basel, Switzerland) · 2025Review
- Discovery Potential Hub Genes and Pathways in Keloid Fibroblast Development Based on Bioinformatics Analysis.International journal of genomics · 2025Article
- TAGLN-RhoA/ROCK2-SLC2A3-mediated Mechano-metabolic Axis Promotes Skin Fibrosis.International journal of biological sciences · 2025Article
- LangerinClinical, cosmetic and investigational dermatology · 2025Review
- LRRC15+ Myofibroblasts as a Stromal State Linking Repair, Fibrosis, and Scarring.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
Keloid is a dermatofibrotic disease known for its aggressive nature and characterized by pathological scarring, which often leads to disfigurement and frequent recurrences. Effective therapies for keloids are still limited, presumably due to the inadequate comprehension of their aggressive mechanisms. In our study, we examined the unique scenario where both keloid and non-aggressive pathological scar originate from the same patient, providing a rare opportunity to explore the aggressive mechanisms of keloids through single-cell RNA sequencing. We found that the dominant fibroblast subgroup in keloids is mechanoresponsive group, which showed enhanced mechanotransduction and migration. This mechanoresponsive fibroblast subgroup is likely to be the key cell population and confer aggressive growth of keloids. The results also indicate that the endothelial cells and keratinocytes in keloid involve in endothelial-mesenchymal and epithelial-mesenchymal transitions. This study demonstrated the mechanoresponsive fibroblasts and multiple cellular mesenchymal processes could pave the way for further investigations into the keloid aggressiveness.
Indexed as
Identifiers
What Socratic holds
Registered trials
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.