Inhibiting scar formation in vitro and in vivo by adenovirus‐mediated mutant Smad4: a preliminary report

No abstract is available for this paper.

• Publication year

  2011

• Venue

  Experimental Dermatology

• Publication date

  2011-02-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1111/j.1600-0625.2010.01186.xPMID 21255090
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• Novel therapies for scar reduction and regenerative healing of skin wounds.

  2008cited by this paper
• Genetic susceptibility to Keloid scarring: SMAD gene SNP frequencies in Afro‐Caribbeans

  2008cited by this paper
• Smad3 null mice display more rapid wound closure and reduced scar formation after a stab wound to the cerebral cortex.

  2007cited by this paper
• Increased CCN2 Transcription in Keloid Fibroblasts Requires Cooperativity Between AP-1 and SMAD Binding Sites

  2007cited by this paper
• Reduction of hypertrophic scar via retroviral delivery of a dominant negative TGF-beta receptor II.

  2007cited by this paper
• Smad3 deficiency alters key structural elements of the extracellular matrix and mechanotransduction of wound closure.

  2006cited by this paper
• Inhibiting Scar Formation in Rat Wounds by Adenovirus-Mediated Overexpression of Truncated TGF-&bgr; Receptor II

  2005cited by this paper
• Ontogeny of expression of transforming growth factor‐β and its receptors and their possible relationship with scarless healing in human fetal skin

  2005cited by this paper
• Increased CCN2 transcription in keloid fibroblasts requires cooperativity between AP-1 and SMAD binding sites.

  2004cited by this paper
• [The influence of the application of cytotoxic lymphocyte antigen 4-Ig adenovirus on the burn wounds with alloskin grafting on the murine immune function].

  2004cited by this paper
• Suppression of transforming growth factor beta/smad signaling in keloid-derived fibroblasts by quercetin: implications for the treatment of excessive scars.

  2004cited by this paper
• Role of Smad4 on TGF-beta-induced extracellular matrix stimulation in mesangial cells.

  2003cited by this paper
• Skin repair and scar formation: the central role of TGF-β

  2003cited by this paper
• Effect of human hepatocyte growth factor on promoting wound healing and preventing scar formation by adenovirus-mediated gene transfer.

  2003cited by this paper
• Transforming growth factor-beta signaling through the Smad pathway: role in extracellular matrix gene expression and regulation.

  2002cited by this paper
• Expression of TGF-beta and its receptors in murine fetal and adult dermal wounds.

  2001cited by this paper
• Constitutive phosphorylation and nuclear localization of Smad3 are correlated with increased collagen gene transcription in activated hepatic stellate cells

  2001cited by this paper
• Loss of Smad3 modulates wound healing.

  2000cited by this paper
• Modulation of endogenous Smad expression in normal skin fibroblasts by transforming growth factor-beta.

  2000cited by this paper
• The Use of Newborn Rats and an Adenoviral Gene Delivery Vector as a Model System for Wound‐Healing Research

  2000cited by this paper
• The Smad4 Activation Domain (SAD) Is a Proline-rich, p300-dependent Transcriptional Activation Domain*

  2000cited by this paper
• Gene therapy in wound repair and regeneration

  2000cited by this paper
• Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response

  1999cited by this paper
• TGF-beta signal transduction.

  1998cited by this paper
• Characterization of Functional Domains within Smad4/DPC4*

  1997cited by this paper
• Adenovirus-mediated Transfer of a Truncated Transforming Growth Factor-β (TGF-β) Type II Receptor Completely and Specifically Abolishes Diverse Signaling by TGF-β in Vascular Wall Cells in Primary Culture*

  1996cited by this paper
• TGFβ Signaling: Receptors, Transducers, and Mad Proteins

  1996cited by this paper
• The effect of TGF-beta on keloid fibroblast proliferation and collagen synthesis.

  1996cited by this paper
• Adenovirus-mediated transfer of a truncated transforming growth factor-beta (TGF-beta) type II receptor completely and specifically abolishes diverse signaling by TGF-beta in vascular wall cells in primary culture.

  1996cited by this paper
• TGFbeta signaling: receptors, transducers, and Mad proteins.

  1996cited by this paper
• Exogenous Transforming Growth Factor‐Beta Amplifies Its Own Expression and Induces Scar Formation in a Model of Human Fetal Skin Repair

  1995cited by this paper
• Neutralising antibody to TGF-beta 1,2 reduces cutaneous scarring in adult rodents.

  1994cited by this paper
• Modulation of Collagen Synthesis by Transforming Growth Factor‐β in Keloid and Hypertrophic Scar Fibroblasts

  1994cited by this paper
• Cells, Matrix, Growth Factors, and the Surgeon The Biology of Scarless Fetal Wound Repair

  1994cited by this paper
• Gene therapy: adenovirus vectors.

  1993cited by this paper
• Fetal fracture healing in a lamb model.

  1992cited by this paper
• A model for fetal cleft lip repair in lambs.

  1992cited by this paper
• Transforming growth factor type beta: rapid induction of fibrosis and angiogenesis in vivo and stimulation of collagen formation in vitro.

  1986cited by this paper

• Topical gel containing Polysiloxanes and hyaluronic acid for skin scar: Formulation design, characterization, and In vivo activity

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• p38MAPK silencing attenuates scar proliferation after cleft palate repair surgery in rats via MRTF-A/SRF pathway.

  2022cites this paper
• Identification of differentially expressed circular RNAs in keloid and normal skin tissue by high‐throughput sequencing

  2021cites this paper
• Co-transfection of hepatocyte growth factor and truncated TGF-β type II receptor inhibit scar formation

  2020cites this paper
• HIF-1α promotes the keloid development through the activation of TGF-β/Smad and TLR4/MyD88/NF-κB pathways

  2019cites this paper
• Current and upcoming therapies to modulate skin scarring and fibrosis.

  2019cites this paper
• Development of a Chitosan-Vaseline Gauze Dressing with Wound-Healing Properties in Murine Models.

  2019cites this paper
• The effect of topical ramipril and losartan cream in inhibiting scar formation.

  2019cites this paper
• Gene Therapy in Reconstructive and Regenerative Surgery

  2018influential citation
• Angiotensin-converting enzyme inhibitor reduces scar formation by inhibiting both canonical and noncanonical TGF-β1 pathways

  2018cites this paper
• Angiotensin‐converting enzyme inhibitor works as a scar formation inhibitor by down‐regulating Smad and TGF‐β‐activated kinase 1 (TAK1) pathways in mice

  2018cites this paper
• Gene Therapy in Pathologic Scars

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• Characterization of Smad3 knockout mouse derived skin cells

  2017cites this paper
• MicroRNAs in Skin Fibrosis

  2015cites this paper
• [Nuclear factor I-C inhibits platelet-derived growth factor-induced enhancement of dermal fibroblast sensitivity to TGF-β].

  2015cites this paper
• Loureirin B inhibits fibroblast proliferation and extracellular matrix deposition in hypertrophic scar via TGF‐β/Smad pathway

  2015cites this paper
• Effect of Chitosan Nanospheres Loaded with VEGF on Adipose Tissue Transplantation: A Preliminary Report

  2014cites this paper
• The Effect of Local Rho-Kinase Inhibition on Murine Wound Healing

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• Effects of TRAP-1-Like Protein (TLP) Gene on Collagen Synthesis Induced by TGF-β/Smad Signaling in Human Dermal Fibroblasts

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• Molecular basis of organ fibrosis: Potential therapeutic approaches

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• A New Minimally Invasive Mesotherapy Technique for Facial Rejuvenation

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• The role of microRNAs in skin fibrosis

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• Bioactive reagents used in mesotherapy for skin rejuvenation in vivo induce diverse physiological processes in human skin fibroblasts in vitro– a pilot study

  2012cites this paper
• Clinical and molecular effects on mature burn scars after treatment with a fractional CO2 laser

  2012cites this paper