ReviewFrontiers in medicine2020
The Network of Inflammatory Mechanisms in Lupus Nephritis.
Review in Frontiers in medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Article
- MALT1 serves as a biomarker for estimating disease risk of lupus nephritis: a prospective case-control study.Annals of translational medicine · 2022Article
- Mesangial Cells in Lupus Nephritis.Current rheumatology reports · 2022Review
- Investigating the Mechanisms of Jieduquyuziyin Prescription Improves Lupus Nephritis and Fibrosis via FXR in MRL/lpr Mice.Oxidative medicine and cellular longevity · 2022Article
- Knockout of the KH-Type Splicing Regulatory Protein Drives Glomerulonephritis in MRL-FasCells · 2021Article
- Deposition of Immune Complexes in Gingival Tissues in the Presence of Periodontitis and Systemic Lupus Erythematosus.Frontiers in immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several signaling pathways are involved in the progression of kidney disease in humans and in animal models, and kidney disease is usually due to the sustained activation of these pathways. Some of the best understood pathways are specific proinflammatory cytokine and protein kinase pathways (e.g., protein kinase C and mitogen-activated kinase pathways, which cause cell proliferation and fibrosis and are associated with angiotensin II) and transforming growth factor-beta (TGF-β) signaling pathways (e.g., the TGF-β signaling pathway, which leads to increased fibrosis and kidney scarring. It is thus necessary to continue to advance our knowledge of the pathogenesis and molecular biology of kidney disease and to develop new treatments. This review provides an update of important findings about kidney diseases (including diabetic nephropathy, lupus nephritis, and vasculitis, i.e., vasculitis with antineutrophilic cytoplasmic antibodies). New disease targets, potential pathological pathways, and promising therapeutic approaches from basic science to clinical practice are presented, and the blocking of JAK/STAT and TIM-1/TIM-4 signaling pathways as potential novel therapeutic agents in lupus nephritis is discussed.
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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.