ReviewFrontiers in medicine2023
Molecular insight in intrarenal inflammation affecting four main types of cells in nephrons in IgA nephropathy.
Review in Frontiers in medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.
- Visceral Obesity and Metabolic Dysfunction in IgA Nephropathy: Nutritional and Metabolic Perspectives on Disease Progression.Nutrients · 2025Pooled it
- Diagnostic potential of B-cell translocation gene 2 in IgA nephropathy: Insights from molecular mechanisms.Journal of cell communication and signaling · 2026Article
- Immunofluorescence Patterns in IgAN are Associated With Active, Necrotizing Lesions.Kidney international reports · 2026Article
- Recent Advances in the Management of IgA Nephropathy: From Supportive Care to Targeted Therapies.Cureus · 2026Review
- Renal Tubular Epithelial Cells as Central Hubs of Kidney Disease.Diagnostics (Basel, Switzerland) · 2026Review
- Single-dose rituximab as induction therapy in adult IgA vasculitis with rapidly progressive glomerulonephritis: a case report with peripheral blood CD19⁺ B-cell monitoring.CEN case reports · 2026Article
- The key role and research progress of endothelial cells in renal microcirculation.Frontiers in medicine · 2026Review
- Pathological characteristics of traditional Chinese medicine Shi Zheng and related therapeutic formula, effective compounds: a general review.Chinese medicine · 2025Review
- Impact of gut microbiota in chronic kidney disease: natural polyphenols as beneficial regulators.Renal failure · 2025Review
- Therapeutic Mechanisms of Jinshuiqing in IgA Nephropathy: A Transcriptomic Analysis.Medical science monitor basic research · 2025Article
- F2RL1 Inhibition Alleviates Lipotoxicity-Induced Kidney Injury Through the Hippo Pathway in Diabetic Kidney Disease.Inflammation · 2025Article
- Inflammation-associated molecules in the glomerular-endothelium in mild IgA-nephropathy patients identified by single-cell and spatial transcriptome.Communications biology · 2025Article
- Blockade of mTOR ameliorates IgA nephropathy by correcting CD89 and CD71 dysfunctions in humanized mice.PloS one · 2025Article
- Renal Health Through Medicine-Food Homology: A Comprehensive Review of Botanical Micronutrients and Their Mechanisms.Nutrients · 2024Review
- Review
- Efficacy and safety of biologic agents for IgA nephropathy: A protocol for systematic review and meta-analysis.PloS one · 2024Article
- [Research advances in the etiology and pathogenesis of immunoglobulin A vasculitis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Review
- Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.Frontiers in immunology · 2023Review
- IgA Nephropathy: Emerging Mechanisms of Disease.Indian journal of nephrologyReview
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunoglobulin A nephropathy (IgAN) is the most common primary glomerulonephritis and the leading cause of kidney failure in the world. The current widely accepted framework for its pathogenesis is the "multi-hit hypothesis." In this review, we mainly discussed the intrarenal inflammation in IgAN, which is initiated by immune complex deposition with complement molecule activation, by focusing on four main types of cells in nephrons including mesangial cells, endothelial cells, podocytes, and tubular epithelial cells (TECs). Galactose-deficient IgA1 (Gd-IgA1)-containing immune complexes deposit in the mesangium and activate complement molecules and mesangial cells. Activation of mesangial cells by Gd-IgA1 deposition with enhanced cellular proliferation, extracellular matrix (ECM) expansion, and inflammatory response plays a central role in the pathogenesis of IgAN. Regional immune complex deposition and mesangial-endothelial crosstalk result in hyperpermeability of endothelium with loss of endothelial cells and infiltration barrier proteins, and recruitment of inflammatory cells. Podocyte damage is mainly derived from mesangial-podocyte crosstalk, in which tumor necrosis factor-α (TNF-α), transforming growth factor-β (TGF-β), renin-angiotensin-aldosterone system (RAAS), and micro-RNAs are the major players in podocyte apoptosis and disorganization of slit diaphragm (SD) related to proteinuria in patients with IgAN. In addition to filtrated proteins into tubulointerstitium and mesangial-tubular crosstalk involved in the injury of TECs, retinoic acid has been discovered innovatively participating in TEC injury.
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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 Socratic graph.