ReviewAmerican journal of physiology. Renal physiology2022
Endothelial cells: potential novel regulators of renal inflammation.
Review in American journal of physiology. Renal physiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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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Who cites it
33 citing papers in PubMed, 45 citations in OpenAlex.
- Metabolic Complications in Autoimmune and Autoinflammatory Diseases: Pathophysiology, Clinical Implications, and Therapeutic Perspectives.Journal of clinical medicine · 2026Review
- Low-dose exposure to organophosphate pesticides and chronic kidney disease: insights from urinary dialkyl phosphate biomarkers.Clinical and experimental nephrology · 2026Article
- Hyperuricemia accelerates renal dysfunction due to hypertensive nephrosclerosis: the TAMA MED Project-CKD.BMC nephrology · 2026Article
- Bmpr2 Drives Aberrant Activation and Injury of Glomerular Endothelial Cells in Lupus Nephritis.Journal of the American Society of Nephrology : JASN · 2026Article
- Advances in research on the mechanisms of anti-inflammation of silybin: a review.Frontiers in immunology · 2026Review
- NO-cGMP Signaling in Endothelial Function of the Healthy and Inflamed Dental Pulp.International journal of molecular sciences · 2025Review
- Galectin-3/CD146 interaction promotes renal damage and systemic inflammation after acute kidney injury.Scientific reports · 2025Article
- Article
- Endothelial dysfunction in chronic kidney disease: a clinical perspective.American journal of physiology. Heart and circulatory physiology · 2025Review
- Inflammation-associated molecules in the glomerular-endothelium in mild IgA-nephropathy patients identified by single-cell and spatial transcriptome.Communications biology · 2025Article
- Lupus nephritis serum induces changes in gene expression in human glomerular endothelial cells, which is modulated by L-sepiapterin: implications for redox-mediated endothelial dysfunction.Lupus science & medicine · 2025Article
- Neutrophils and NETs in kidney disease.Nature reviews. Nephrology · 2025Review
- Microvascular aberrations found in human polycystic kidneys are an early feature in a Pkd1 mutant mouse model.Disease models & mechanisms · 2025Article
- ADAMTS13 attenuates renal fibrosis by suppressing thrombospondin 1 mediated TGF-β1/Smad3 activation.Toxicology and applied pharmacology · 2025Article
- Recent advances on immunity and hypertension: the new cells on the kidney block.American journal of physiology. Renal physiology · 2025Review
- Targeting Trichloroethylene-Induced Renal Endothelial Cell Injuries: A Role of Poly I:C in Amplification of HMGB1 Acetylation.Journal of toxicology · 2025Article
- Targeting endothelial cells: the pathological mechanisms and therapeutic innovations in pulmonary arterial hypertension.Frontiers in cell and developmental biology · 2025Review
- Role of Uremic Toxins in Vascular Inflammation Associated with Chronic Kidney Disease.Journal of clinical medicine · 2024Article
- Epigenetics of Hypertensive Nephropathy.Biomedicines · 2024Review
- Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Substantial evidence has supported the role of endothelial cell (EC) activation and dysfunction in the development of hypertension, chronic kidney disease (CKD), and lupus nephritis (LN). In both humans and experimental models of hypertension, CKD, and LN, ECs become activated and release potent mediators of inflammation including cytokines, chemokines, and reactive oxygen species that cause EC dysfunction, tissue damage, and fibrosis. Factors that activate the endothelium include inflammatory cytokines, mechanical stretch, and pathological shear stress. These signals can activate the endothelium to promote upregulation of adhesion molecules, such as intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, which promote leukocyte adhesion and migration to the activated endothelium. More importantly, it is now recognized that some of these signals may in turn promote endothelial antigen presentation through major histocompatibility complex II. In this review, we will consider in-depth mechanisms of endothelial activation and the novel mechanism of endothelial antigen presentation. Moreover, we will discuss these proinflammatory events in renal pathologies and consider possible new therapeutic approaches to limit the untoward effects of endothelial inflammation in hypertension, CKD, and LN.
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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.