ArticleJCI insight2022
Oxidative stress promotes fibrosis in systemic sclerosis through stabilization of a kinase-phosphatase complex.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 12 citations in OpenAlex.
- Noncoding RNA TY1 reverses fibrosis in systemic sclerosis by attenuating the cGAS/STING pathway.JCI insight · 2026Article
- Th17-related genes PGAP1 and TMBIM1 serve as potential diagnostic and predictive biomarkers in systemic sclerosis: bioinformatic identification and murine model validation.Clinical rheumatology · 2026Article
- The research progress on the role of glucose-6-phosphate dehydrogenase in immune regulation.PeerJ · 2026Review
- Endothelial and platelet dysfunction in systemic sclerosis with pulmonary hypertension.PloS one · 2026Article
- The Role of Abatacept on Inflammation and Fibrosis in Hypochlorous Acid-Induced Fibrosis Mice.International journal of rheumatic diseases · 2025Article
- Deciphering myocardial fibrosis: a comprehensive bibliometric analysis of mechanism over the period 1992-2023.Journal of cardiothoracic surgery · 2025Article
- A review of recent studies on the pathogenesis of Systemic Sclerosis: focus on fibrosis pathways.Frontiers in immunology · 2025Review
- Interrelation of Natural Polyphenol and Fibrosis in Diabetic Nephropathy.Molecules (Basel, Switzerland) · 2024Review
- Preparation of Oxidized and Reduced PTP4A1 for Structural and Functional Studies.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Journey into the Esophageal Complications: Decoding Systemic Sclerosis with Cutting-Edge Endoscopy, Manometry, and Ambulatory pH-Study.International journal of general medicine · 2024Article
- Ozone Pollution, Oxidative Stress, Regulatory T Cells and Antioxidants.Antioxidants (Basel, Switzerland) · 2022Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
Abstract
Systemic sclerosis (SSc) is a fibrotic autoimmune disease characterized by pathogenic activation of fibroblasts enhanced by local oxidative stress. The tyrosine phosphatase PTP4A1 was identified as a critical promoter of TGF-β signaling in SSc. Oxidative stress is known to functionally inactivate tyrosine phosphatases. Here, we assessed whether oxidation of PTP4A1 modulates its profibrotic action and found that PTP4A1 forms a complex with the kinase SRC in scleroderma fibroblasts, but surprisingly, oxidative stress enhanced rather than reduced PTP4A1's association with SRC and its profibrotic action. Through structural assessment of the oxo-PTP4A1-SRC complex, we unraveled an unexpected mechanism whereby oxidation of a tyrosine phosphatase promotes its function through modification of its protein complex. Considering the importance of oxidative stress in the pathogenesis of SSc and fibrosis, our findings suggest routes for leveraging PTP4A1 oxidation as a potential strategy for developing antifibrotic agents.
Indexed as
Identifiers
What Socratic 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 Socratic graph.