ReviewJournal of nephrology2017
Toll-like receptor-4 signaling mediates inflammation and tissue injury in diabetic nephropathy.
Review in Journal of nephrology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 95 citations in OpenAlex.
- Monocyte dipeptidyl peptidase 4 activity is associated with urinary albumin excretion in type 2 diabetes.Journal of diabetes investigation · 2026Article
- Hydroxysafflor yellow A improves diabetes-induced renal fibrosis.Archives of medical science : AMS · 2026Article
- Host-pathogen interactions in periodontitis: an integrative interkingdom perspective.Frontiers in immunology · 2026Review
- The TRIM14-KIF1B Axis Drives Renal Injury in Diabetic Nephropathy Through TLR4/NF-κB Pathway Modulation.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Semaglutide Enhances Cellular Regeneration in Skin and Retinal Cells In Vitro.Pharmaceutics · 2025Article
- Network Pharmacology, Molecular Dynamics Simulation, and Biological Validation Insights into the Potential of Ligustri Lucidi Fructus for Diabetic Nephropathy.International journal of molecular sciences · 2025Article
- Regulation of pyroptosis in diabetic nephropathy by long non-coding and circular RNAs.Clinical and experimental medicine · 2025Review
- Reactive Oxygen Species in Asthma: Regulators of Macrophage Polarization and Therapeutic Implications: A Narrative Review.Journal of asthma and allergy · 2025Review
- Research on TCM Comprehensive Treatment of DKD Based on Pathophysiological Mechanism.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Natural compounds improve diabetic nephropathy by regulating the TLR4 signaling pathway.Journal of pharmaceutical analysis · 2024Review
- Anti-inflammatory benefits of semaglutide: State of the art.Journal of clinical & translational endocrinology · 2024Review
- Jianpi Gushen Huayu decoction ameliorated diabetic nephropathy through modulating metabolites in kidney, and inhibiting TLR4/NF-κB/NLRP3 and JNK/P38 pathways.World journal of diabetes · 2024Article
- Personalizing Nutrition Strategies: Bridging Research and Public Health.Journal of personalized medicine · 2024Review
- SA-β-Gal in Kidney Tubules as a Predictor of Renal Outcome in Patients with Chronic Kidney Disease.Journal of clinical medicine · 2024Article
- The role of innate immunity in diabetic nephropathy and their therapeutic consequences.Journal of pharmaceutical analysis · 2024Review
- Sodium Glucose Transporter-2 Inhibitors (SGLT2Is)-TLRs Axis Modulates Diabetes.Cell biochemistry and biophysics · 2023Review
- Mitochondrial Impairment: A Link for Inflammatory Responses Activation in the Cardiorenal Syndrome Type 4.International journal of molecular sciences · 2023Review
- Identifying Aging-Related Biomarkers and Immune Infiltration Features in Diabetic Nephropathy Using Integrative Bioinformatics Approaches and Machine-Learning Strategies.Biomedicines · 2023Article
- Review
- LncRNA SNHG16 regulates RAS and NF-κB pathway-mediated NLRP3 inflammasome activation to aggravate diabetes nephropathy through stabilizing TLR4.Acta diabetologica · 2023Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Toll-like receptors (TLRs) are a class of receptors of the innate immune system which detect pathogen-associated and danger-associated molecular patterns in order to initiate an inflammatory response. TLR2 and TLR4 downward signaling causes the production of proinflammatory cytokines that can induce insulin resistance and cardiovascular damage in obesity and type 2 diabetes mellitus. In diabetic nephropathy, TLR4, nucleotide-binding oligomerization domain-containing protein 2 (NOD2), and NLRP3 inflammasome are involved in the production and persistence of inflammation. The activation of TLRs stimulates the expression of several inflammatory cytokines and chemokines such as CCL2 and tumor necrosis factor (TNF)-α, which are associated with the progression of diabetic nephropathy. Different inflammatory mechanisms seem to take place in the early and late stages of diabetic kidney disease, with activation of the innate immunity response and enhanced chemiotactic effects in native kidney cells at an early stage, followed by tubulointerstitial monocyte infiltration at a more advanced disease state. Overall, available data indicate that the upregulated TLR4 response in the kidney translates the metabolic alterations of diabetes into kidney damage.
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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.