ArticleScientific reports2015
Hypertrophic scar contracture is mediated by the TRPC3 mechanical force transducer via NFkB activation.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- Evidence-based therapy in hypertrophic scars: An update of a systematic review.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2020Pooled it
- Transient Receptor Potential (TRP) Channels as Fundamental Regulators of Fibrosis and Pruritus-A New Therapeutic Target for Pathological Scar Management.International journal of molecular sciences · 2026Review
- Modulating hypertrophic scar formation by targeting endothelial transient receptor potential vanilloid-1/nuclear factor kappa-B/interleukin-6 axis to regulate angiogenesis.Burns & trauma · 2026Article
- Propolis compound inhibits profibrotic TGF-β1/SMAD signalling in human fibroblasts.Scientific reports · 2025Article
- Specific Calcium Signal Responses in Human Keloid-Derived Fibroblasts During Cyclical Stretching: Basic Research.Health science reports · 2025Article
- Canonical transient receptor potential channel 1 aggravates myocardial ischemia-and-reperfusion injury by upregulating reactive oxygen species.Journal of pharmaceutical analysis · 2023Article
- Gallic Acid Treats Hypertrophic Scar in Rabbit Ears via the TGF-β/Smad and TRPC3 Signaling Pathways.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Impaired healing of cutaneous wound in a Trpv1 deficient mouse.Experimental animals · 2023Article
- Stretching Promotes Wound Contraction Through Enhanced Expression of Endothelin Receptor B and TRPC3 in Fibroblasts.Plastic and reconstructive surgery. Global open · 2023Article
- Multimodal roles of transient receptor potential channel activation in inducing pathological tissue scarification.Frontiers in immunology · 2023Review
- Healing Mechanisms in Cutaneous Wounds: Tipping the Balance.Tissue engineering. Part B, Reviews · 2022Review
- Skin biomechanics: a potential therapeutic intervention target to reduce scarring.Burns & trauma · 2022Review
- Mechanotransduction in skin wound healing and scar formation: Potential therapeutic targets for controlling hypertrophic scarring.Frontiers in immunology · 2022Review
- Expression of NF-κB-p65 and α-SMA in the Study of Capsules formed by Surface Textured Implants Versus Foam Covered Silicone Implants in a Rat Model.World journal of plastic surgery · 2021Article
- [Roles of interleukin-6/signal transduction and activator of transcription 3 pathway andZhonghua shao shang za zhi = Zhonghua shaoshang zazhi = Chinese journal of burns · 2021Article
- Article
- Mechanobiological Feedback in Pulmonary Vascular Disease.Frontiers in physiology · 2018Review
- Inflammatory cytokine IL6 cooperates with CUDR to aggravate hepatocyte-like stem cells malignant transformation through NF-κB signaling.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Wound healing process is a complex and highly orchestrated process that ultimately results in the formation of scar tissue. Hypertrophic scar contracture is considered to be a pathologic and exaggerated wound healing response that is known to be triggered by repetitive mechanical forces. We now show that Transient Receptor Potential (TRP) C3 regulates the expression of fibronectin, a key regulatory molecule involved in the wound healing process, in response to mechanical strain via the NFkB pathway. TRPC3 is highly expressed in human hypertrophic scar tissue and mechanical stimuli are known to upregulate TRPC3 expression in human skin fibroblasts in vitro. TRPC3 overexpressing fibroblasts subjected to repetitive stretching forces showed robust expression levels of fibronectin. Furthermore, mechanical stretching of TRPC3 overexpressing fibroblasts induced the activation of nuclear factor-kappa B (NFκB), a regulator fibronectin expression, which was able to be attenuated by pharmacologic blockade of either TRPC3 or NFκB. Finally, transplantation of TRPC3 overexpressing fibroblasts into mice promoted wound contraction and increased fibronectin levels in vivo. These observations demonstrate that mechanical stretching drives fibronectin expression via the TRPC3-NFkB axis, leading to intractable wound contracture. This model explains how mechanical strain on cutaneous wounds might contribute to pathologic scarring.
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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.