ArticleMolecular medicine (Cambridge, Mass.)2024
ADAM Metallopeptidase domain 19 promotes skin fibrosis in systemic sclerosis via neuregulin-1.
Article in Molecular medicine (Cambridge, Mass.), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- ADAM19: biological characteristics and implications in disease pathology and clinical applications.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
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- Long-term cytokine exposure remodels the methylome and transcriptome of recessive dystrophic epidermolysis bullosa keratinocytes - a bioinformatic analysis.Frontiers in cell and developmental biology · 2026Article
- Integrative Analysis of Telomere-Related Genes Reveals Prognostic Signatures in Laryngeal Cancer.International journal of genomics · 2026Article
- Identification and validation of mitochondrial transport and glycolysis-associated prognostic and therapeutic target for lung adenocarcinoma patients.Frontiers in genetics · 2026Article
- Integrative analysis of cuproptosis in kidney ischemia-reperfusion injury: biomarker discovery and diagnostic model construction.Frontiers in molecular biosciences · 2026Article
- Prognostic and immunological implications of sialylation-associated gene signatures in hepatocellular carcinoma.Annals of medicine · 2025Article
- Low-intensity pulsed ultrasound attenuates atrial remodelling and atrial fibrillation after myocardial infarction: an experimental pre-clinical study.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025Article
- Identification and single-cell analysis of prognostic genes related to mitochondrial and neutrophil extracellular traps in bladder cancer.Scientific reports · 2025Article
- The J-shaped association between the ratio of neutrophil counts to prognostic nutritional index and mortality in ICU patients with sepsis: a retrospective study based on the MIMIC database.Frontiers in cellular and infection microbiology · 2025Article
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13 authors.
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Abstract
backgroundADAM19 (ADAM Metallopeptidase Domain 19) is known to be involved in extracellular matrix (ECM) remodeling, yet its specific function in systemic sclerosis (SSc) fibrosis remains unclear.
objectivesThis study sought to clarify the role and underlying mechanism of ADAM19 in SSc skin fibrosis.
methodsThe expression of ADAM19 was assessed in skin tissues of SSc and wound healing using publicly available transcriptome datasets. This analysis was further validated through real-time PCR, western blot, and immunostaining in our SSc cohort, as well as in a mouse model of hypochlorite (HOCl)-induced fibrosis. To downregulate the expression of ADAM19, ADAM19 siRNA was employed. The influence of ADAM19 on fibroblast transcriptomics was examined using bulk RNA-seq. Data analysis and visualization were conducted using R packages, including edgeR, limma, clusterProfiler, ggplot2, gseaplot2, and complexheatmap.
resultsADAM19 exhibited a significant upregulation in skin tissues of SSc patients, as well as in wound healing and a HOCl-induced fibrosis mouse model. Additionally, there was a notable positive correlation between ADAM19 and fibrosis-related genes, local skin score, Modified Rodnan skin score, skin thickness progression rate, and the presence of ARA antibodies in SSc patients. Furthermore, ADAM19 levels were markedly elevated in SSc primary dermal fibroblasts and TGF-β-stimulated healthy controls primary dermal fibroblasts. The downregulation of ADAM19 resulted in the repression of TGF-β-induced ECM deposition and fibroblast activation. ADAM19 was identified as a mediator for the shedding of neuregulin-1 (NRG1) in fibroblasts, a pro-fibrotic cytokine that must be cleaved to exert its function.
conclusionADAM19 plays a role in TGF-β-induced ECM deposition and fibroblast activation by mediating the shedding of NRG1, ultimately contributing to the development of skin fibrosis in SSc.
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