ReviewCurrent rheumatology reports2002
Apoptosis and myofibroblasts in the pathogenesis of systemic sclerosis.
Review in Current rheumatology reports, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 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
15 citing papers in PubMed, 41 citations in OpenAlex.
- Halofuginone suppresses hepcidin by a heparan sulfate-dependent mechanism to treat iron disorders in mice.Blood advances · 2026Article
- Salirasib Inhibits the Expression of Genes Involved in Fibrosis in Fibroblasts of Systemic Sclerosis Patients.Immunity, inflammation and disease · 2024Article
- The Role of Autophagy and Apoptosis in Affected Skin and Lungs in Patients with Systemic Sclerosis.International journal of molecular sciences · 2023Review
- The Roles of Noncoding RNAs in Systemic Sclerosis.Frontiers in immunology · 2022Review
- Novel Concepts in Systemic Sclerosis Pathogenesis: Role for miRNAs.Biomedicines · 2021Review
- The Inter-α-Trypsin Inhibitor Family: Versatile Molecules in Biology and Pathology.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2020Review
- Expression of apoptotic and proliferation factors in gastric mucosa of patients with systemic sclerosis correlates with form of the disease.Scientific reports · 2019Article
- Myocardial fibrosis in congenital and pediatric heart disease.Experimental and therapeutic medicine · 2017Article
- Neuroinflammatory Mechanisms of Connective Tissue Fibrosis: Targeting Neurogenic and Mast Cell Contributions.Advances in wound care · 2015Review
- Myofibroblasts: trust your heart and let fate decide.Journal of molecular and cellular cardiology · 2014Review
- Systemic sclerosis sera affect fibrillin-1 deposition by dermal blood microvascular endothelial cells: therapeutic implications of cyclophosphamide.Arthritis research & therapy · 2013Article
- Relaxin: antifibrotic properties and effects in models of disease.Clinical medicine & research · 2005Review
- Mast cells in the pathogenesis of fibrosis.Current rheumatology reports · 2003Review
- Exosomes isolated from serum of systemic sclerosis patients display alterations in their content of profibrotic and antifibrotic microRNA and induce a profibrotic phenotype in cultured normal dermal fibroblasts.Clinical and experimental rheumatologyArticle
- Serum amyloid P inhibits dermal wound healing.Wound repair and regeneration : official publication of the Wound Healing Society [and] the European Tissue Repair SocietyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tissue fibrosis is the result of a complex series of events focusing on regulation of fibroblast proliferation, synthesis of extracellular matrix, and apoptosis. Transforming growth factor-beta is important for the stimulation of the fibrotic response by promoting the production of extracellular matrix proteins, by promoting the differentiation of the myofibroblast cell morphology, and by protecting these cells against apoptotic stimuli. Other cytokines such as interleukin-1 may have stimulatory and counter-regulatory effects on fibrosis. The effects of these signaling molecules depend on cellular environment and are organ specific. Furthermore, intercellular interactions and cell-matrix interactions can stimulate or inhibit the apoptotic pathway. Through selective inhibition of apoptosis in myofibroblasts, fibrosis can become dysregulated and lead to diseases such as systemic sclerosis.
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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.