ArticleCell death & disease2022
Complement induces podocyte pyroptosis in membranous nephropathy by mediating mitochondrial dysfunction.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
45 citing papers in PubMed, 56 citations in OpenAlex.
- Macrophage pyroptosis in lupus nephritis - Novel insights into renal pathogenesis and clinical correlates: A cross-sectional study.Medicine · 2026Observational
- Animal models of idiopathic membranous nephropathy: Recent advances and future perspectives.Animal models and experimental medicine · 2026Review
- Proteomic Profiling of Complement Components in Glomerular Disease.Laboratory investigation; a journal of technical methods and pathology · 2026Article
- Podocyte Metabolic Reprogramming and Targeted Therapy.Journal of the American Society of Nephrology : JASN · 2026Review
- The lipid-podocyte axis: emerging clues in membranous nephropathy pathogenesis.Frontiers in medicine · 2026Review
- Navigating renal safety in the biologic treatment of psoriasis: from immunologic mechanisms to clinical practice.Frontiers in immunology · 2026Review
- Immune podocyte injury in autoimmune glomerular diseases.Frontiers in immunology · 2026Review
- Mitochondrial abnormalities in nondiabetic and nonhypertensive glomerular diseases: a comprehensive review.Molecular and cellular biochemistry · 2026Review
- Programmed Cell Death: A Key Mechanism of Traditional Chinese Medicine in the Treatment of Membranous Nephropathy.Drug design, development and therapy · 2026Review
- Exploring the mechanism by which modified huangqi chifeng decoction protects podocytes via Arid5a-mediated transcriptional regulation of the AIM2 pyroptosis signaling axis.Frontiers in immunology · 2026Article
- SIRT6 Attenuates Angiotensin II-Induced Podocyte Cholesterol Accumulation and Injury via Negative Modulation of SREBP2.Kidney & blood pressure research · 2026Article
- Immune mechanisms and immunomodulatory therapies in steroid-resistant nephrotic syndrome.Renal failure · 2025Review
- Pyroptosis-induced tissue damage in kidney disease.Renal failure · 2025Review
- Complement C3 in panvascular disease: a central integrator of immune signaling and vascular remodeling.Clinical science (London, England : 1979) · 2025Review
- Nicotinism vs. Glomerulopathies-Smoking as a Risk Factor for Primary Glomerulopathies.Antioxidants (Basel, Switzerland) · 2025Review
- Exploring the Role of TRAF6-TAK1 Pathway in Podocyte Pyroptosis and Its Implications for Primary Membranous Nephropathy Therapy.Inflammation · 2025Article
- Intercepting the complement amplification loop through podocyte MC5R signaling ameliorates membranous nephropathy.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Mechanisms and Therapeutic Perspectives of Podocyte Aging in Podocytopathies.International journal of molecular sciences · 2025Review
- Article
- The crucial role of neutrophil extracellular traps and IL-17 signaling in indomethacin-induced gastric injury in mice.Scientific reports · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocyte damage mediated by in situ complement activation in the glomeruli is a key factor in the pathogenesis of membranous nephropathy (MN), but the molecular mechanism has not been fully elucidated. Pyroptosis is a special type of programmed cell death, mediate inflammatory response and induce tissue injury. However, it is not clear whether pyroptosis is involved in the development and progression of MN. Here, we report that pyroptosis plays an important role in promoting podocyte injury in MN. We first observed the occurrence of pyroptosis in the kidneys of MN patients and validated that complement stimulation triggered pyroptosis in podocytes and that inhibiting pyroptosis reversed complement-induced podocyte damage in vitro. In addition, stimulation of complement caused mitochondrial depolarization and reactive oxygen species (ROS) production in podocytes, and inhibition of ROS reversed complement-induced pyroptosis in podocytes. Interestingly, inhibition of pyroptosis in turn partially alleviated these effects. Furthermore, we also found the involvement of pyroptosis in the kidneys of passive Heymann nephritis (PHN) rats, and inhibitors of pyroptosis-related molecules relieved PHN-induced kidney damage in vivo. Our findings demonstrate that pyroptosis plays a critical role in complement-induced podocyte damage in MN and mitochondrial dysfunction is an important mechanism underlying this process. It provides new insight that pyroptosis may serve as a novel therapeutic target for MN treatment in future studies.
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.