ArticleThe American journal of pathology2010
alpha2-antiplasmin is associated with the progression of fibrosis.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.
What it found
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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.
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Who cites it
16 citing papers in PubMed, 26 citations in OpenAlex.
- Pathogenic and Regulatory Roles of Fibrinolytic Factors in Autoimmune Diseases.Current issues in molecular biology · 2025Review
- Review
- The uPA/uPAR System Orchestrates the Inflammatory Response, Vascular Homeostasis, and Immune System in Fibrosis Progression.International journal of molecular sciences · 2023Review
- α2-Antiplasmin as a Potential Therapeutic Target for Systemic Sclerosis.Life (Basel, Switzerland) · 2022Review
- α2-antiplasmin positively regulates endothelial-to-mesenchymal transition and fibrosis progression in diabetic nephropathy.Molecular biology reports · 2022Article
- Article
- MicroRNA-30c attenuates fibrosis progression and vascular dysfunction in systemic sclerosis model mice.Molecular biology reports · 2021Article
- α2AP is associated with the development of lupus nephritis through the regulation of plasmin inhibition and inflammatory responses.Immunity, inflammation and disease · 2020Article
- Alternatively activated macrophages are associated with the α2AP production that occurs with the development of dermal fibrosis : The role of alternatively activated macrophages on the development of fibrosis.Arthritis research & therapy · 2020Article
- The Role of Fibrinolytic Regulators in Vascular Dysfunction of Systemic Sclerosis.International journal of molecular sciences · 2019Review
- α2AP regulates vascular alteration by inhibiting VEGF signaling in systemic sclerosis: the roles of α2AP in vascular dysfunction in systemic sclerosis.Arthritis research & therapy · 2017Article
- Pathogenesis of Systemic Sclerosis.Frontiers in immunology · 2015Review
- α2AP mediated myofibroblast formation and the development of renal fibrosis in unilateral ureteral obstruction.Scientific reports · 2014Article
- Article
- Plasminogen/plasmin modulates bone metabolism by regulating the osteoblast and osteoclast function.The Journal of biological chemistry · 2011Article
- Pulmonary arterial hypertension patients display normal kinetics of clot formation using thrombelastography.Pulmonary circulationArticle
Corrections and comments
- Erratum issued
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic sclerosis results in tissue fibrosis due to the activation of fibroblasts and the ensuing overproduction of the extracellular matrix. We previously reported that the absence of alpha2-antiplasmin (alpha2AP) attenuated the process of dermal fibrosis; however, the detailed mechanism of how alpha2AP affects the progression of fibrosis remained unclear. The goal of the present study was to examine the role of alpha2AP in fibrotic change. We observed significantly higher levels of alpha2AP expression in the skin of bleomycin-injected systemic sclerosis model mice in comparison with the levels seen in control mice. We also demonstrated that alpha2AP induced myofibroblast differentiation, and the absence of alpha2AP attenuated the induction of myofibroblast differentiation. Moreover, we found that connective tissue growth factor induced the expression of alpha2AP through both the extracellular signal-regulated kinase 1/2 (ERK1/2) and c-Jun N-terminal kinase (JNK) pathways in fibroblasts. Interestingly, alpha2AP also induced transforming growth factor-beta expression through the same pathways, and the inhibition of ERK1/2 and JNK slowed the progression of bleomycin-induced fibrosis. Our findings suggest that alpha2AP is associated with the progression of fibrosis, and regulation of alpha2AP expression by the ERK1/2 and JNK pathways may be an effective antifibrotic therapy for the treatment of systemic sclerosis.
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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.