ReviewMolecular medicine reports2023
Immune podocytes in the immune microenvironment of lupus nephritis (Review).
Review in Molecular medicine reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis 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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Pooled it
- IgG Glycosylation-Dependent CLEC7A Signaling Drives Podocyte Dysfunction in Lupus Nephritis.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Exosomal immune decoy integrates cfDNA scavenging and mTOR inhibition for synergistic lupus nephritis therapy.Theranostics · 2026Article
- The chemokine network in lupus nephritis: pathogenesis, targeted therapies, and future directions.Frontiers in pharmacology · 2026Review
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- GBP2 promotes podocyte pyroptosis and contributes to the pathogenesis of pediatric lupus nephritis.PloS one · 2026Article
- Autoantibody repertoire in lupus nephritis: from pathogenic mechanisms to clinical integration for precision decision-making.Frontiers in immunology · 2026Review
- Long non-coding RNA NEAT1 mediated lupus nephritis induced podocytes pyroptosis through DNMT1-STING axis.Renal failure · 2025Article
- The Spectrum of Minimal Change Disease/Focal Segmental Glomerulosclerosis: From Pathogenesis to Proteomic Biomarker Research.International journal of molecular sciences · 2025Review
- Imbalance of T cell subsets: a core event that mediates the progression of T2DM and its complications.Frontiers in immunology · 2025Review
- Podocyte, tubular epithelial-immune cell interplay in the pathogenesis of lupus nephritis.Frontiers in immunology · 2025Review
- Exosomes secreted by podocytes regulate the differentiation of Th17/Treg cells in idiopathic nephrotic syndrome.Heliyon · 2024Article
- Lupus Nephritis from Pathogenesis to New Therapies: An Update.International journal of molecular sciences · 2024Review
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- Changes in macrophage infiltration and podocyte injury in lupus nephritis patients with repeated renal biopsy: Report of three cases.World journal of clinical cases · 2024Article
- Influence of Podocyte Injury on the Development of Class IV Lupus Nephritis.International journal of nephrology and renovascular disease · 2024Article
- Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.Frontiers in immunology · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic lupus erythematosus (SLE) is a systemic autoimmune disorder caused by the loss of tolerance to endogenous nuclear antigens such as double‑stranded DNA, leading to the proliferation of T cells and subsequent activation of B cells, which results in serious organ damage and life‑threatening complications such as lupus nephritis. Lupus nephritis (LN) develops as a frequent complication of SLE, accounting for >60% of SLE cases, and is characterized by proteinuria and heterogeneous histopathological findings. Glomerular injury serves a role in proteinuria as podocyte damage is the leading contributor. Numerous studies have reported that podocytes are involved in the immune response that promotes LN progression. In LN, immune complex deposition stimulates dendritic cells to secrete inflammatory cytokines that activate T cells and B cells. B cells secrete autoantibodies that attack and damage the renal podocytes, leading to renal podocyte injury. The injured podocytes trigger inflammatory cells through the expression of toll‑like receptors and trigger T cells through major histocompatibility complexes and CD86, thereby participating in the local immune response and the exacerbation of podocyte injury. Based on the existing literature, the present review summarizes the research progress of podocytes in LN under the local immune microenvironment of the kidney, explores the mechanism of podocyte injury under the immune microenvironment, and evaluates podocytes as a potential therapeutic target for LN.
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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.