ArticleAmerican journal of physiology. Renal physiology2018
Podocytes contribute, and respond, to the inflammatory environment in lupus nephritis.
Article in American journal of physiology. Renal physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 48 citations in OpenAlex.
- Ginsenoside Compound K Mitigates Mitochondrial Fission Through Bile Acid Receptors/YAP Signaling to Counteract Podocyte Injury in Lupus Nephritis.Phytotherapy research : PTR · 2026Article
- From Genes to Pathways: The Molecular Landscape of Systemic Lupus Erythematosus.International journal of molecular sciences · 2026Review
- Enhanced WWP2 Exacerbates Podocyte Injury in Lupus Nephritis through Monoubiquitylating H2A at K119.International journal of biological sciences · 2026Article
- Long non-coding RNA NEAT1 mediated lupus nephritis induced podocytes pyroptosis through DNMT1-STING axis.Renal failure · 2025Article
- Podocyte extracellular vesicles and immune mediators as urinary biomarkers in active lupus nephritis.Scientific reports · 2025Article
- Identification of serum exosomal miRNA biomarkers in patients with lupus nephritis.Clinical rheumatology · 2025Article
- Article
- Mechanistic Insights Into Redox Damage of the Podocyte in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2025Review
- Inflammation in glomerular diseases.Frontiers in immunology · 2025Review
- Breaking the cycle: immune complexes, complement activation, and novel immunotherapies in lupus nephritis.Frontiers in immunology · 2025Review
- The immunoregulatory roles of non-haematopoietic cells in the kidney.Nature reviews. Nephrology · 2024Review
- Swollen Feet: Considering the Paradoxical Roles of Interleukins in Nephrotic Syndrome.Biomedicines · 2024Review
- Central role of podocytes in mediating cellular cross talk in glomerular health and disease.American journal of physiology. Renal physiology · 2024Review
- Reciprocal regulation of SIRT1 and AMPK by Ginsenoside compound K impedes the conversion from plasma cells to mitigate for podocyte injury in MRL/Journal of ginseng research · 2024Article
- Complement Activation in Nephrotic Glomerular Diseases.Biomedicines · 2024Review
- Influence of Podocyte Injury on the Development of Class IV Lupus Nephritis.International journal of nephrology and renovascular disease · 2024Article
- Immune podocytes in the immune microenvironment of lupus nephritis (Review).Molecular medicine reports · 2023Review
- Pathogenic cellular and molecular mediators in lupus nephritis.Nature reviews. Nephrology · 2023Review
- Safety of CAR-T Cell Therapy in Patients With Renal Failure/Acute Kidney Injury: Focused Review.Clinical hematology international · 2023Review
- New insights into the immune functions of podocytes: the role of complement.Molecular and cellular pediatrics · 2023Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Lupus nephritis (LN) affects up to 80% of juvenile onset systemic lupus erythematosus patients, leading to end stage renal failure requiring dialysis or transplantation in 10-15%. Podocytes are specialized epithelial cells of the glomerulus known to be a key site of damage in glomerular diseases. However, their roles in LN have yet to be fully identified. This project aims to identify structural and functional roles of podocytes in an in vitro model of LN. Conditionally immortalized podocytes were treated with proinflammatory cytokines (IL-1β, TNF-α, IFN-α, and IFN-γ) alone and in combination in an in vitro model of LN and were assessed for their structural and functional characteristics. Podocytes produce TNF-α, IL-6, IL-8, VEGF, granulocyte-monocyte colony stimulating factor (GM-CSF), and macrophage colony stimulating factor (M-CSF) at relatively low levels under basal conditions; stimulation with IL-1β led to increased secretion of IL-6 ( P = 0.011), IL-8 ( P = 0.05), VEGF ( P = 0.02), and M-CSF ( P = 0.03). Stimulation with TNF-α led to increased secretion of M-CSF ( P = 0.049) and stimulation with IFN-γ led to novel production of IL-10 ( P = 0.036) and interferon-γ-inducible protein-10 ( P = 0.036). Podocytes demonstrate a reduction in the area covered by filamentous-actin in response to IL-1β treatment within 1 h ( P = 0.011), which is restored by 24 h, associated with an increase in the level of intracellular calcium but not with increased cell death. Podocytes contribute to the inflammatory milieu in LN through cytokine/chemokine secretion and respond to the inflammatory milieu via rearrangement of the actin cytoskeleton leading to effacement, a well-known method of protection against apoptosis in these cells. This demonstrates that podocytes are involved in the pathogenesis of LN.
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