ReviewISRN rheumatology2013
Role of endothelial to mesenchymal transition in the pathogenesis of the vascular alterations in systemic sclerosis.
Review in ISRN rheumatology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.
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
65 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- 3D-Mesenchymal stromal cells derived VASH2 alleviates oxidative stress-induced endothelial senescence by mediating α-tubulin detyrosination in systemic sclerosis.Journal of translational medicine · 2026Article
- Micro- and Macro-Vascular Disease in Systemic Sclerosis and Very Early SSc (VEDOSS): Results from a Monocentric Observational Study.Biomedicines · 2026Article
- Systemic Sclerosis: A Key Model of Endothelial Dysfunction.Biomedicines · 2025Review
- Characterization of Circulating Vesicles of Complicated and Uncomplicated Systemic Sclerosis Patients and Their Role in Vascular Dysfunction.International journal of molecular sciences · 2025Article
- An updated overview of Juvenile systemic sclerosis in a French cohort.Pediatric rheumatology online journal · 2025Article
- Systems-based identification of the Hippo pathway for promoting fibrotic mesenchymal differentiation in systemic sclerosis.Nature communications · 2024Article
- Endothelial Dysfunction in Systemic Sclerosis.International journal of molecular sciences · 2023Review
- A Narrative Review of Pathogenetic and Histopathologic Aspects, Epidemiology, Classification Systems, and Disease Outcome Measures in Systemic Sclerosis.Clinical reviews in allergy & immunology · 2023Review
- Immune and Non-Immune Inflammatory Cells Involved in Autoimmune Fibrosis: New Discoveries.Journal of clinical medicine · 2023Review
- M2 macrophage polarization in systemic sclerosis fibrosis: pathogenic mechanisms and therapeutic effects.Heliyon · 2023Review
- Endothelial-to-mesenchymal transition: An underappreciated mediator of diabetic complications.Frontiers in endocrinology · 2023Review
- Gut microbe-derived metabolite trimethylamine N-oxide activates PERK to drive fibrogenic mesenchymal differentiation.iScience · 2022Article
- Serum lysyl oxidase concentration increases in long-standing systemic sclerosis: Can lysyl oxidase change over time?Archives of rheumatology · 2022Article
- Effects ofFood science & nutrition · 2022Article
- Systemic Sclerosis: From Pathophysiology to Novel Therapeutic Approaches.Biomedicines · 2022Review
- Cell Based Treatment of Autoimmune Diseases in Children.Frontiers in pediatrics · 2022Review
- Contributions of Immune Cells and Stromal Cells to the Pathogenesis of Systemic Sclerosis: Recent Insights.Frontiers in pharmacology · 2022Review
- Global gene expression analysis of systemic sclerosis myofibroblasts demonstrates a marked increase in the expression of multiple NBPF genes.Scientific reports · 2021Article
- Iloprost Attenuates Oxidative Stress-Dependent Activation of Collagen Synthesis Induced by Sera from Scleroderma Patients in Human Pulmonary Microvascular Endothelial Cells.Molecules (Basel, Switzerland) · 2021Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of Systemic Sclerosis (SSc) is extremely complex, and despite extensive studies, the exact mechanisms involved are not well understood. Numerous recent studies of early events in SSc pathogenesis have suggested that unknown etiologic factors in a genetically receptive host trigger structural and functional microvascular endothelial cell abnormalities. These alterations result in the attraction, transmigration, and accumulation of immune and inflammatory cells in the perivascular tissues, which in turn induce the phenotypic conversion of endothelial cells and quiescent fibroblasts into activated myofibroblasts, a process known as endothelial to mesenchymal transition or EndoMT. The activated myofibroblasts are the effector cells responsible for the severe and frequently progressive fibrotic process and the fibroproliferative vasculopathy that are the hallmarks of SSc. Thus, according to this hypothesis the endothelial and vascular alterations, which include the phenotypic conversion of endothelial cells into activated myofibroblasts, play a crucial role in the development of the progressive fibrotic process affecting skin and multiple internal organs. The role of endothelial cell and vascular alterations, the potential contribution of endothelial to mesenchymal cell transition in the pathogenesis of the tissue fibrosis, and fibroproliferative vasculopathy in SSc will be reviewed here.
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.