ReviewClinical & developmental immunology2013
Mediators of inflammation and their effect on resident renal cells: implications in lupus nephritis.
Review in Clinical & developmental immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 43 citations in OpenAlex.
- Long-Term Safety and Efficacy of Belimumab in Patients With Systemic Lupus Erythematosus: A Continuation of a Seventy-Six-Week Phase III Parent Study in the United States.Arthritis & rheumatology (Hoboken, N.J.) · 2018Trial
- Long-term organ damage accrual and safety in patients with SLE treated with belimumab plus standard of care.Lupus · 2016Trial
- FGF23-related hypophosphatemic rickets preceding the onset of systemic lupus erythematosus: A juvenile case.Clinical case reports · 2024Article
- Decipher the Immunopathological Mechanisms and Set Up Potential Therapeutic Strategies for Patients with Lupus Nephritis.International journal of molecular sciences · 2023Review
- Mesangial cell: A hub in lupus nephritis.Frontiers in immunology · 2022Review
- Kidney Tertiary Lymphoid Structures in Lupus Nephritis Develop into Large Interconnected Networks and Resemble Lymph Nodes in Gene Signature.The American journal of pathology · 2020Article
- α2AP is associated with the development of lupus nephritis through the regulation of plasmin inhibition and inflammatory responses.Immunity, inflammation and disease · 2020Article
- 1,4-Disubstituted 1International journal of molecular sciences · 2020Article
- Identification of Renal Long Non-coding RNA RP11-2B6.2 as a Positive Regulator of Type I Interferon Signaling Pathway in Lupus Nephritis.Frontiers in immunology · 2019Article
- Altered renal immune complexes deposition in female BWF1 lupus mice followingSaudi journal of biological sciences · 2018Article
- Sophocarpine attenuates murine lupus nephritis via inhibiting NLRP3 inflammasome and NF-κB activation.Immunologic research · 2018Article
- T cells and autoimmune kidney disease.Nature reviews. Nephrology · 2017Review
- Urinary markers in the early stage of nephropathy in patients with childhood-onset type 1 diabetes.Pediatric nephrology (Berlin, Germany) · 2016Article
- Cytokines: Names and Numbers You Should Care About.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
- Article
- MicroRNA Profiling of B Cell Subsets from Systemic Lupus Erythematosus Patients Reveals Promising Novel Biomarkers.International journal of molecular sciences · 2015Article
- NKG2D ligand overexpression in lupus nephritis correlates with increased NK cell activity and differentiation in kidneys but not in the periphery.Journal of leukocyte biology · 2015Article
- Tumor necrosis factor-α synergistically enhances polyinosinic-polycytidylic acid-induced toll-like receptor 3 signaling in cultured normal human mesangial cells: possible involvement in the pathogenesis of lupus nephritis.Clinical and experimental nephrology · 2015Article
- Demethylzeylasteral (T-96) Treatment Ameliorates Mice Lupus Nephritis Accompanied by Inhibiting Activation of NF-κB Pathway.PloS one · 2015Article
- Regulation of synthesis and roles of hyaluronan in peritoneal dialysis.BioMed research international · 2015Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lupus nephritis affects up to 70% of patients with systemic lupus erythematosus and is a major cause of morbidity and mortality. It is characterized by a breakdown of immune tolerance, production of autoantibodies, and deposition of immune complexes within the kidney parenchyma, resulting in local inflammation and subsequent organ damage. To date, numerous mediators of inflammation have been implicated in the development and progression of lupus nephritis, and these include cytokines, chemokines, and glycosaminoglycans. Of these, type I interferons (IFNs) can increase both gene and protein expression of cytokines and chemokines associated with lupus susceptibility, and interleukin-6 (IL-6), tumor necrosis factor- α (TNF- α ) and hyaluronan have been shown to elicit both pro- and anti-inflammatory effects on infiltrating and resident renal cells depending on the status of their microenvironment. Expression of IL-6, TNF- α , type I IFNs, and hyaluronan are increased in the kidneys of patients and mice with active lupus nephritis and have been shown to contribute to disease pathogenesis. There is also evidence that despite clinical remission, ongoing inflammatory processes may occur within the glomerular and tubulointerstitial compartments of the kidney, which further promote kidney injury. In this review, we provide an overview of the synthesis and putative roles of IL-6, TNF- α , IFN- α , and hyaluronan in the pathogenesis of lupus nephritis focusing on their effects on human mesangial cells and proximal renal tubular epithelial cells.
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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.