ArticleEMBO molecular medicine2021
Pro-inflammatory immunity supports fibrosis advancement in epidermolysis bullosa: intervention with Ang-(1-7).
Article in EMBO molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 50 citations in OpenAlex.
- Trophoblast Extracellular Vesicles Rewire Immunity: A Symptom-Relief Avenue for Recessive Dystrophic Epidermolysis Bullosa.Journal of extracellular vesicles · 2026Article
- Dermal papillary fibroblasts promote persistent granulation tissue formation in junctional epidermolysis bullosa.EMBO molecular medicine · 2026Article
- Systemic clinical-grade recombinant decorin reduces disease burden and fibrosis in advanced recessive dystrophic epidermolysis bullosa.Molecular therapy. Advances · 2026Article
- SOX2 Is a Potential Diagnostic Biomarker and Anticancer Target in Cutaneous Squamous Cell Carcinoma in Dystrophic Epidermolysis Bullosa: A Case Series Study.JID innovations : skin science from molecules to population health · 2026Article
- miR-129-1-3p down-regulation promotes BAG cochaperone 3 (BAG3)-driven pro-fibrotic processes in primary fibroblasts from patients with recessive dystrophic epidermolysis bullosa.Non-coding RNA research · 2025Article
- Inflammatory modulation by cord blood stem cells prevented digit deformation in recessive dystrophic epidermolysis bullosa.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The Role of Fibroblasts in Dystrophic Epidermolysis Bullosa Pathogenesis and Current Treatment Approaches.JID innovations : skin science from molecules to population health · 2025Review
- Paw Skin as a Translational Model for Investigating Fibrotic and Inflammatory Wound Healing Defects in Recessive Dystrophic Epidermolysis Bullosa.International journal of molecular sciences · 2025Article
- Advances in Extracellular Matrix-Associated Diagnostics and Therapeutics.Journal of clinical medicine · 2025Review
- Skin Deep and Beyond: Unravelling B Cell Extracellular Matrix Interactions in Cutaneous Immunity and Disease.Experimental dermatology · 2025Review
- The Differentiation and Regeneration Potential of ABCB5Journal of clinical medicine · 2025Review
- Systems immunology integrates the complex endotypes of recessive dystrophic epidermolysis bullosa.Nature communications · 2025Article
- Safety and tolerability of losartan to treat recessive dystrophic epidermolysis bullosa in children (REFLECT): an open-label, single-arm, phase 1/2 trial.EClinicalMedicine · 2024Article
- Angiotensin (1-7) Inhibits Transforming Growth Factor-Β1-Induced Epithelial-Mesenchymal Transition of Human Keratinocyte Hacat Cells in vitro.Clinical, cosmetic and investigational dermatology · 2024Article
- Fibrosis as a Risk Factor for Cutaneous Squamous Cell Carcinoma in Recessive Dystrophic Epidermolysis Bullosa: A Systematic Review.Journal of pediatric genetics · 2023Review
- Kinetics of Wound Development and Healing Suggests a Skin-Stabilizing Effect of Allogeneic ABCB5Cells · 2023Article
- Maintenance of chronicity signatures in fibroblasts isolated from recessive dystrophic epidermolysis bullosa chronic wound dressings under culture conditions.Biological research · 2023Article
- Inflammation-mediated fibroblast activation and immune dysregulation in collagen VII-deficient skin.Frontiers in immunology · 2023Article
- Deconstructing progressive inflammatory fibrosis in recessive dystrophic epidermolysis bullosa.EMBO molecular medicine · 2021Article
- Pro-inflammatory immunity supports fibrosis advancement in epidermolysis bullosa: intervention with Ang-(1-7).EMBO molecular medicine · 2021Article
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16 authors at 3 institutions in 3 countries.
Funding
Abstract
Recessive dystrophic epidermolysis bullosa (RDEB), a genetic skin blistering disease, is a paradigmatic condition of tissue fragility-driven multi-organ fibrosis. Here, longitudinal analyses of the tissue proteome through the course of naturally developing disease in RDEB mice revealed that increased pro-inflammatory immunity associates with fibrosis evolution. Mechanistically, this fibrosis is a consequence of altered extracellular matrix organization rather than that of increased abundance of major structural proteins. In a humanized system of disease progression, we targeted inflammatory cell fibroblast communication with Ang-(1-7)-an anti-inflammatory heptapeptide of the renin-angiotensin system, which reduced the fibrosis-evoking aptitude of RDEB cells. In vivo, systemic administration of Ang-(1-7) efficiently attenuated progression of multi-organ fibrosis and increased survival of RDEB mice. Collectively, our study shows that selective down-modulation of pro-inflammatory immunity may mitigate injury-induced fibrosis. Furthermore, together with published data, our data highlight molecular diversity among fibrotic conditions. Both findings have direct implications for the design of therapies addressing skin fragility and fibrosis.
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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.