ArticleThe Journal of investigative dermatology2008
Hic-5 promotes the hypertrophic scar myofibroblast phenotype by regulating the TGF-beta1 autocrine loop.
Article in The Journal of investigative dermatology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
44 citing papers in PubMed, 73 citations in OpenAlex.
- Hic-5 drives epithelial mechanotransduction promoting a feed-forward cycle of bronchoconstriction.Nature communications · 2025Article
- A comparative analysis of paxillin and Hic-5 proximity interactomes.Cytoskeleton (Hoboken, N.J.) · 2025Article
- Hic-5 regulates extracellular matrix-associated gene expression and cytokine secretion in cancer associated fibroblasts.Experimental cell research · 2024Article
- Molecular and metabolomic characterization of hiPSC-derived cardiac fibroblasts transitioning to myofibroblasts.Frontiers in cell and developmental biology · 2024Article
- The Role of Tenascin-C in Hypertrophic Scar Formation: Insights from Cell and Animal Experiments.Clinical, cosmetic and investigational dermatology · 2024Article
- Physiological and pathological roles of Hic‑5 in several organs (Review).International journal of molecular medicine · 2022Review
- Review
- Transdermal delivery of Chinese herbal medicine extract using dissolvable microneedles for hypertrophic scar treatment.Acta pharmaceutica Sinica. B · 2021Article
- Fibroblasts: Heterogeneous Cells With Potential in Regenerative Therapy for Scarless Wound Healing.Frontiers in cell and developmental biology · 2021Review
- A Metabolic Reprogramming of Glycolysis and Glutamine Metabolism Is a Requisite for Renal Fibrogenesis-Why and How?Frontiers in physiology · 2021Review
- Paxillin family of focal adhesion adaptor proteins and regulation of cancer cell invasion.International review of cell and molecular biology · 2020Article
- The focal adhesion scaffold protein Hic-5 regulates vimentin organization in fibroblasts.Molecular biology of the cell · 2019Article
- Molecular determinants of mesenchymal cell activation in fibroproliferative diseases.Cellular and molecular life sciences : CMLS · 2019Review
- Angiotensin-converting enzyme inhibitor works as a scar formation inhibitor by down-regulating Smad and TGF-β-activated kinase 1 (TAK1) pathways in mice.British journal of pharmacology · 2018Article
- The impact of stromal Hic-5 on the tumorigenesis of colorectal cancer through lysyl oxidase induction and stromal remodeling.Oncogene · 2018Article
- Signaling Mechanisms of Myofibroblastic Activation: Outside-in and Inside-Out.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2018Review
- Article
- Current concepts related to hypertrophic scarring in burn injuries.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair Society · 2016Review
- Hic-5 is required for myofibroblast differentiation by regulating mechanically dependent MRTF-A nuclear accumulation.Journal of cell science · 2016Article
- Dermal Fibroblasts from the Red Duroc Pig Have an Inherently Fibrogenic Phenotype: An In Vitro Model of Fibroproliferative Scarring.Plastic and reconstructive surgery · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Following severe traumatic or thermal injury to the dermis, hypertrophic scars (HTSs) often develop in humans. These scar fibroblasts (hypertrophic scar fibroblasts (HTSFs)) retain the myofibroblast phenotype persistently, rather than transiently as in acute wounds. These pathogenic myofibroblasts constitutively express smooth-muscle cell alpha-actin (SMAA), deposit an excessive amount of extracellular matrix (ECM) proteins, are highly contractile, and stably display large focal adhesions. Increasing evidence supports a mechanism in which autocrine production and activation of transforming growth factor-beta1 (TGF-beta1) are required to maintain the pathogenic myofibroblast phenotype. We recently reported that Hic-5, a focal adhesion protein that is upregulated by TGF-beta1, is expressed persistently in HTSF compared to normal adult fibroblasts (NADFs). We now find that Hic-5 is an important regulator of the constitutive myofibroblast phenotype in HTSFs. Silencing the expression of Hic-5 in HTSFs with specific siRNAs dramatically reduces TGF-beta1 production, decreases the generation of supermature focal adhesions reduces expression of SMAA and decreases collagen contraction and ECM synthesis. Our findings demonstrate that Hic-5 is an essential component of the mechanism regulating autocrine production of TGF-beta1 and the resulting pathogenic myofibroblast phenotype.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.