ReviewNature reviews. Nephrology2016
Innate immunity in diabetes and diabetic nephropathy.
Review in Nature reviews. Nephrology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 255 papers, 4 of them syntheses that pooled it.
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
255 citing papers in PubMed, 4 syntheses or guidelines pooled it, 422 citations in OpenAlex.
- From Mechanism to Therapy: Isoliquiritigenin as a Novel Anti-Inflammatory Agent for Inflammatory Disease ManagementEndocrine, metabolic & immune disorders drug targets · 2026Pooled it
- Epidemiological linkage between migraine and diabetes mellitus: a systematic review and meta-analysis.The journal of headache and pain · 2024Pooled it
- The Specific Alteration of Gut Microbiota in Diabetic Kidney Diseases-A Systematic Review and Meta-Analysis.Frontiers in immunology · 2022Pooled it
- Effects of valsartan combined with α-lipoic acid on renal function in patients with diabetic nephropathy: a systematic review and meta-analysis.BMC endocrine disorders · 2021Pooled it
- Antimicrobial Peptides for Diabetic Foot Ulcers and Infections: Current Evidence and Translational Perspectives.International journal of molecular sciences · 2026Review
- Characterizing the Immune Cell Infiltration in Renal Interstitium and Therapeutic Targets of Drugs in Diabetic Nephropathy by Multiomics Study.Diabetes & metabolism journal · 2026Article
- Immune cell phenotypes in the context of diabetic nephropathy: A Mendelian randomization analysis.Medicine · 2026Article
- Defective efferocytosis in diabetes: molecular mechanisms and emerging therapeutic strategies.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- AARS1 promotes diabetic kidney disease through rewiring Akt and NF-κB signaling to suppress autophagy and sustain inflammation.Cellular & molecular biology letters · 2026Article
- The role of immunoproteasome in diabetes and diabetes-related complications.Genes & diseases · 2026Review
- Podocyte TLR4 deletion alleviates diabetic kidney disease through prohibiting PKCδ/SHP-1-dependent ER stress and relieving podocyte damage and inflammation.Journal of advanced research · 2026Article
- Advanced Glycation End-Products Contribute to Delayed Diabetic Corneal Epithelial Wound Healing via the TLR4 Signaling.Investigative ophthalmology & visual science · 2026Article
- DUSP1 Attenuates Renal Injury in Diabetic Nephropathy by Modulating Ferroptosis: Evidence From Animal Experiments.Immunity, inflammation and disease · 2026Article
- Progress on Omega-3 fatty acids for the comprehensive and targeted treatment of spinal cord injury.Bone research · 2026Review
- Therapeutic Opportunities for Macrophage Targeted Nanomedicine in Diabetes Mellitus.International journal of nanomedicine · 2026Review
- Integrated single-cell transcriptomic and machine-learning analyses identify a CD36-associated macrophage state in diabetic nephropathy.Frontiers in immunology · 2026Article
- Single Cell and Spatial Transcriptomics Define a Proinflammatory and Profibrotic Niche After Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Competing Risks Analysis for Neutrophil to Lymphocyte Ratio as a Predictor of Diabetic Nephropathy Incidence.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Article
- Epidemiological and transcriptome data identify potential key genes involved in inflammatory response for diabetic nephropathy.Scientific reports · 2025Article
- Diagnostic immune-related markers for diabetic kidney disease: a bioinformatics and machine learning approach.Renal failure · 2025Article
195 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate immune system includes several classes of pattern recognition receptors (PRRs), including membrane-bound Toll-like receptors (TLRs) and nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs). These receptors detect pathogen-associated molecular patterns (PAMPs) and danger-associated molecular patterns (DAMPs) in the extracellular and intracellular space. Intracellular NLRs constitute inflammasomes, which activate and release caspase-1, IL-1β, and IL-18 thereby initiating an inflammatory response. Systemic and local low-grade inflammation and release of proinflammatory cytokines are implicated in the development and progression of diabetes mellitus and diabetic nephropathy. TLR2, TLR4, and the NLRP3 inflammasome can induce the production of various proinflammatory cytokines and are critically involved in inflammatory responses in pancreatic islets, and in adipose, liver and kidney tissues. This Review describes how innate immune system-driven inflammatory processes can lead to apoptosis, tissue fibrosis, and organ dysfunction resulting in insulin resistance, impaired insulin secretion, and renal failure. We propose that careful targeting of TLR2, TLR4, and NLRP3 signalling pathways could be beneficial for the treatment of diabetes mellitus and diabetic nephropathy.
Indexed as
Identifiers
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.