ArticleEBioMedicine2015
Mitochondrial-dependent Autoimmunity in Membranous Nephropathy of IgG4-related Disease.
Article in EBioMedicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Comparison of the efficacy of low, moderate and standard doses of rituximab in the treatment of membranous nephropathy.Frontiers in medicine · 2026Article
- Oxidative Stress and Nutritional Antioxidants in Renal Diseases: A Narrative Review.Antioxidants (Basel, Switzerland) · 2025Review
- Antibodies Against Anti-Oxidant Enzymes in Autoimmune Glomerulonephritis and in Antibody-Mediated Graft Rejection.Antioxidants (Basel, Switzerland) · 2024Article
- Technology Innovation for Discovering Renal Autoantibodies in Autoimmune Conditions.International journal of molecular sciences · 2024Review
- Immunoglobulin G4-related disease presenting with nephrotic syndrome due to minimal change disease: a case report.Journal of medical case reports · 2024Article
- Novel biomarkers and pathophysiology of membranous nephropathy: PLA2R and beyond.Clinical kidney journal · 2024Review
- Bi-specific autoantigen-T cell engagers as targeted immunotherapy for autoreactive B cell depletion in autoimmune diseases.Frontiers in immunology · 2024Article
- SARS-CoV-2 spike protein induces lung endothelial cell dysfunction and thrombo-inflammation depending on the C3a/C3a receptor signalling.Scientific reports · 2023Article
- Mechanisms Limiting Renal Tissue Protection and Repair in Glomerulonephritis.International journal of molecular sciences · 2023Review
- Discovery of anti-Formin-like 1 protein (FMNL1) antibodies in membranous nephropathy and other glomerular diseases.Scientific reports · 2022Article
- IgG4 Autoantibodies in Organ-Specific Autoimmunopathies: Reviewing Class Switching, Antibody-Producing Cells, and Specific Immunotherapies.Frontiers in immunology · 2022Review
- Jianpi Qushi Heluo Formula alleviates renal damages in Passive Hemann nephritis in rats by upregulating Parkin-mediated mitochondrial autophagy.Scientific reports · 2021Article
- Renal Involvement in IgG4-Related Disease: From Sunlight to Twilight.Frontiers in medicine · 2021Article
- Mitochondrial dysfunction in kidney injury, inflammation, and disease: Potential therapeutic approaches.Kidney research and clinical practice · 2020Review
- Clinical Manifestations and Long-term Outcomes of IgG4-Related Kidney and Retroperitoneal Involvement in a United Kingdom IgG4-Related Disease Cohort.Kidney international reports · 2019Article
- Response to immunosuppressive therapy in PLABMC nephrology · 2017Article
- Autoantibodies against thrombospondin type 1 domain-containing 7A induce membranous nephropathy.The Journal of clinical investigation · 2016Article
- Idiopathic Retroperitoneal Fibrosis.Journal of the American Society of Nephrology : JASN · 2016Review
- Antibodies to Type IV Collagen Induce Type 1 Autoimmune Pancreatitis.Inflammation · 2016Article
- Membranous Nephropathy: The Journey Continues ….EBioMedicine · 2015Article
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Authors and funding
16 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathophysiology of glomerular lesions of membranous nephropathy (MN), including seldom-reported IgG4-related disease, is still elusive. Unlike in idiopathic MN where IgG4 prevails, in this patient IgG3 was predominant in glomerular deposits in the absence of circulating anti-phospholipase A2 receptor antibodies, suggesting a distinct pathologic process. Here we documented that IgG4 retrieved from the serum of our propositus reacted against carbonic anhydrase II (CAII) at the podocyte surface. In patient's biopsy, glomerular CAII staining increased and co-localized with subepithelial IgG4 deposits along the capillary walls. Patient's IgG4 caused a drop in cell pH followed by mitochondrial dysfunction, excessive ROS production and cytoskeletal reorganization in cultured podocytes. These events promoted mitochondrial superoxide-dismutase-2 (SOD2) externalization on the plasma membrane, becoming recognizable by complement-binding IgG3 anti-SOD2. Among patients with IgG4-related disease only sera of those with IgG4 anti-CAII antibodies caused low intracellular pH and mitochondrial alterations underlying SOD2 externalization. Circulating IgG4 anti-CAII can cause podocyte injury through processes of intracellular acidification, mitochondrial oxidative stress and neoantigen induction in patients with IgG4 related disease. The onset of MN in a subset of patients could be due to IgG4 antibodies recognizing CAII with consequent exposure of mitochondrial neoantigen in the context of multifactorial pathogenesis of disease.
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