ReviewFrontiers in pharmacology2022
Biomechanical Regulatory Factors and Therapeutic Targets in Keloid Fibrosis.
Review in Frontiers in pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 57 citations in OpenAlex.
- Targeted-Penetrating Biomimetic Hybrid Transfersomes for Enhanced Transdermal Gene Transfection in Hypertrophic Scar Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- POSTN(+) fibroblasts and SPP1(+) macrophages in scar formation: A review of mechanisms and therapeutic targets (Review).Molecular medicine reports · 2026Review
- Adjuvant Radiotherapy Following Surgical Excision of Keloids: A Systematic Review of Dose, Fractionation, and Recurrence.Life (Basel, Switzerland) · 2026Review
- Cancer-associated fibroblast-derived stanniocalcin 1 promotes cholangiocarcinoma progression and lymph node metastasis.Fundamental research · 2026Article
- Decoding elastin-collagen resemblance in keloid scar through label-free imaging and machine learning.Journal of biomedical optics · 2026Article
- The Microbial Profile of Keloid Tissue: A Potential Biomarker for Lesion Activity.Biomedicines · 2026Article
- Research Advances in Therapeutic Strategies and Drug Delivery Systems for Pathological Scars.Pharmaceutics · 2026Review
- Identification and histological validation of autophagy-related core genes ADRB2 and PLK2 in keloids, with integrated immune infiltration analysis.Frontiers in immunology · 2026Article
- Transcriptomic analysis reveals that BVDV alters immune and metabolic responses toFrontiers in veterinary science · 2026Article
- From mechanosensing to immune regulation: mechanisms of acupuncture signal initiation and amplification mediated by macrophages.Frontiers in immunology · 2026Review
- Deciphering the cellular landscape of pathological scars.Burns & trauma · 2026Article
- Targeting macrophage function with botulinum toxin: a novel translational strategy for preventing and treating pathological scars.Postepy dermatologii i alergologii · 2026Review
- A panoramic analysis of keloid pathogenesis: multidimensional network regulation of genetics-immunity-metabolism-mechanical force.Frontiers in immunology · 2026Review
- Mechanistic insights into Strontium-90 superficial radiotherapy in keloids: senescence-associated changes and ECM remodeling across cell-matrix scales.Frontiers in pharmacology · 2026Article
- CLICs Inhibitor IAA94 Alleviates Inflammation and Injury in Septic Liver by Preventing Pyroptosis in Macrophages.Inflammation · 2025Article
- Thermoresponsive BrushGel Microcarriers for Efficient Cell Expansion and Enzyme-Reduced Harvesting.Advanced healthcare materials · 2025Article
- Optimal Mechanical Stretch Promotes TSP-1 Expression Through Akt and GSK-3β/β-Catenin Signaling Pathways in Keloid Formation.Health science reports · 2025Article
- Retrospective study comparing three approaches for keloids: surgery + radiotherapy, surgery + pharmacological injection, and surgery alone.BMC surgery · 2025Observational
- Identification of potential biomarkers and mechanisms for keloid disorder based on comprehensive bioinformatics analysis and machine learning algorithms.BMC medical genomics · 2025Article
- ALKBH5 Inhibits YTHDF2-m6A-Mediated Degradation of RCN1 mRNA to Promote Keloid Formation by Activating IRE1α-XBP1-Mediated ER Stress.Journal of cosmetic dermatology · 2025Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Keloids are fibroproliferative skin disorder caused by abnormal healing of injured or irritated skin and are characterized by excessive extracellular matrix (ECM) synthesis and deposition, which results in excessive collagen disorders and calcinosis, increasing the remodeling and stiffness of keloid matrix. The pathogenesis of keloid is very complex, and may include changes in cell function, genetics, inflammation, and other factors. In this review, we aim to discuss the role of biomechanical factors in keloid formation. Mechanical stimulation can lead to excessive proliferation of wound fibroblasts, deposition of ECM, secretion of more pro-fibrosis factors, and continuous increase of keloid matrix stiffness. Matrix mechanics resulting from increased matrix stiffness further activates the fibrotic phenotype of keloid fibroblasts, thus forming a loop that continuously invades the surrounding normal tissue. In this process, mechanical force is one of the initial factors of keloid formation, and matrix mechanics leads to further keloid development. Next, we summarized the mechanotransduction pathways involved in the formation of keloids, such as TGF-β/Smad signaling pathway, integrin signaling pathway, YAP/TAZ signaling pathway, and calcium ion pathway. Finally, some potential biomechanics-based therapeutic concepts and strategies are described in detail. Taken together, these findings underscore the importance of biomechanical factors in the formation and progression of keloids and highlight their regulatory value. These findings may help facilitate the development of pharmacological interventions that can ultimately prevent and reduce keloid formation and progression.
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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 OpenQuestion graph.