ReviewCurrent rheumatology reports2011
A unifying hypothesis for scleroderma: identifying a target cell for scleroderma.
Review in Current rheumatology reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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
10 citing papers in PubMed, 19 citations in OpenAlex.
- RGS5 as a Biomarker of Pericytes, Involvement in Vascular Remodeling and Pulmonary Arterial Hypertension.Vascular health and risk management · 2023Article
- Single-cell RNA-seq reveals the communications between extracellular matrix-related components and Schwann cells contributing to the earlobe keloid formation.Frontiers in medicine · 2022Article
- Molecular mechanisms underlying therapeutic potential of pericytes.Journal of biomedical science · 2018Review
- Vascular Leaking, a Pivotal and Early Pathogenetic Event in Systemic Sclerosis: Should the Door Be Closed?Frontiers in immunology · 2018Review
- Pericytes, microvasular dysfunction, and chronic rejection.Transplantation · 2015Review
- Cellular interactions in the pathogenesis of interstitial lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2015Review
- Type-1 pericytes accumulate after tissue injury and produce collagen in an organ-dependent manner.Stem cell research & therapy · 2014Article
- Vascular leak is a central feature in the pathogenesis of systemic sclerosis.The Journal of rheumatology · 2012Article
- The adventitia: a progenitor cell niche for the vessel wall.Cells, tissues, organs · 2012Review
- NETs: the missing link between cell death and systemic autoimmune diseases?Frontiers in immunology · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We propose that a recent change in the conception of the role of type 1 interferon and the identification of adventitial stem cells suggests a unifying hypothesis for scleroderma. This hypothesis begins with vasospasm. Vasospasm is fully reversible unless, as proposed here, the resulting ischemia leads to apoptosis and activation of type 1 interferon. The interferon, we propose, initiates immune amplification, including characteristic scleroderma-specific antibodies. We propose that the interferon also acts on adventitial stem cells, producing myofibroblasts, rarefaction, and intimal hyperplasia--three morphologic changes that characterize this disease. Regulator of G-protein signaling 5 (RGS5), a regulator of vasoactive G-protein-coupled receptors, is a cell type-specific marker of pericytes and scleroderma myofibroblasts. RGS5 may provide a key link between initial hyperplasia and fibrosis in this disease.
Indexed as
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.