ReviewAmerican journal of physiology. Cell physiology2024
Permissive role of vascular endothelium in fibrosis: focus on the kidney.
Review in American journal of physiology. Cell physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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.
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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
14 citing papers in PubMed, 10 citations in OpenAlex.
- Microvascular autophagy and caspase-3 activation are central regulators of renal fibrosis after ischemia-reperfusion.JCI insight · 2026Article
- 25(OH)D modifies the relationship between depressive symptoms and chronic kidney disease in diabetic patients.International urology and nephrology · 2026Article
- Data-independent acquisition-mass spectrometry proteomic analysis reveals fibrinogen α, β, and γ chains as candidate biomarkers for the nonmaturation of autogenous arteriovenous fistula.International urology and nephrology · 2026Article
- Cardiomyocyte-derived HSPB1 regulates TGF-β1 maturation and inhibits endothelial-to-mesenchymal transition in myocardial fibrosis.iScience · 2026Article
- Association between cumulative changes of the C-reactive protein-triglyceride glucose index and the incidence of rapid kidney function decline: a nationwide prospective cohort study.Frontiers in nutrition · 2026Article
- The key role and research progress of endothelial cells in renal microcirculation.Frontiers in medicine · 2026Review
- Submacular tissue repair and fibrosis in neovascular macular degeneration: A predictable outcome secondary to a chronic age-related endotheliopathy.Molecular vision · 2026Review
- New insights into the mechanism of microvascular rarefaction via endothelial-mesenchymal transition in steroid-induced osteonecrosis of femoral head.Scientific reports · 2025Article
- Integrating Senescence and Oxidative Stress in Cardiac Disease.International journal of molecular sciences · 2025Review
- Targeting long non-coding RNAMolecular therapy. Nucleic acids · 2025Article
- Single-cell analysis of human fibrous dysplasia bone reveals a fibrotic transcriptome and GNAS variants in endothelial, perivascular, and stromal cells.American journal of human genetics · 2025Article
- CCN2 Activates Cellular Senescence Leading to Kidney Fibrosis in Folic Acid-Induced Experimental Nephropathy.International journal of molecular sciences · 2025Article
- Engineering IL-10 and rapamycin to bind collagen leads to improved anti fibrotic efficacy in lung and kidney fibrosis.Scientific reports · 2025Article
- Heterogeneity of Renal Endothelial Cells, Interact with Neighboring Cells, and Endothelial Injury in Chronic Kidney Disease: Mechanisms and Therapeutic Implications.International journal of medical sciences · 2025Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
Fibrosis, the morphologic end-result of a plethora of chronic conditions and the scorch for organ function, has been thoroughly investigated. One aspect of its development and progression, namely the permissive role of vascular endothelium, has been overshadowed by studies into (myo)fibroblasts and TGF-β; thus, it is the subject of the present review. It has been established that tensile forces of the extracellular matrix acting on cells are a prerequisite for mechanochemical coupling, leading to liberation of TGF-β and formation of myofibroblasts. Increased tensile forces are prompted by elevated vascular permeability in response to diverse stressors, resulting in the exudation of fibronectin, fibrinogen/fibrin, and other proteins, all stiffening the extracellular matrix. These processes lead to the development of endothelial cells dysfunction, endothelial-to-mesenchymal transition, premature senescence of endothelial cells, perturbation of blood flow, and gradual obliteration of microvasculature, leaving behind "string" vessels. The resulting microvascular rarefaction is not only a constant companion of fibrosis but also an adjunct mechanism of its progression. The deepening knowledge of the above chain of pathogenetic events involving endothelial cells, namely increased permeability-stiffening of the matrix-endothelial dysfunction-microvascular rarefaction-tissue fibrosis, may provide a roadmap for therapeutic interventions deemed to curtail and reverse fibrosis.
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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.