ReviewFrontiers in immunology2026
Immune podocyte injury in autoimmune glomerular diseases.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Recent key advances in the understanding of the pathogenesis of childhood minimal change disease.Childhood kidney diseases · 2026Review
- Integrated Transcriptomic and Machine Learning Analyses Identify KCNN3 and TLR10 as Candidate Cell-Type-Associated Molecules in Idiopathic Membranous Nephropathy.International journal of general medicine · 2026Article
- Immunotherapy of membranous nephropathy: strategic evolution from CD20 monoclonal antibodies to future vaccines.Frontiers in immunology · 2026Review
- Cellular senescence of renal tubular epithelial cells in diabetic kidney disease: emerging mechanisms and targeted interventions.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune glomerular diseases (AGDs) are immune dysregulation-driven disorders of the glomerulus and a major cause of chronic kidney disease (CKD) and end-stage kidney disease (ESKD). The glomerular filtration barrier, formed by fenestrated endothelial cells, podocytes, and the glomerular basement membrane (GBM), is indispensable for renal homeostasis. Podocytes are terminally differentiated epithelial cells and are difficult to replace once injured. In susceptible individuals, maladaptive activation of humoral and cellular immunity promotes autoantibody formation, immune complex deposition, and complement activation within the glomerulus, leading to early proteinuria and progressive loss of kidney function. Across clinically heterogeneous AGDs, podocytes represent a key convergence point at which immune effector signals are translated into structural and functional barrier failure. Accumulating evidence further suggests that podocytes are not merely passive targets but active "immune podocytes" capable of engaging innate danger-sensing pathways and adopting adaptive immune-like programs that shape local inflammation and disease evolution. This Review synthesizes current advances in immune-mediated podocyte injury, with emphasis on complement-linked signaling, podocyte-intrinsic inflammatory circuits, and podocyte-associated immune interactions. We relate these mechanisms to cytoskeletal remodeling, organelle stress, and regulated cell-death pathways that culminate in podocyte depletion and glomerulosclerosis. We also discuss podocyte protective responses and emerging opportunities for precision, podocyte-centered therapeutics to improve long-term outcomes in AGDs.
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Registered trials
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