ArticleFrontiers in immunology2026
INPP5D/SHIP1-mediated immunometabolic remodeling of renal monocytes in idiopathic membranous nephropathy.
Article 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 2 papers.
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2 citing papers in PubMed.
- Identification of chondroitin polymerizing factor as a biomarker for predicting immunotherapy response in breast cancer: a bioinformatics analysis of tumor microenvironment.Translational cancer research · 2026Article
- Programmed Cell Death: A Key Mechanism of Traditional Chinese Medicine in the Treatment of Membranous Nephropathy.Drug design, development and therapy · 2026Review
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7 authors.
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Abstract
Background: Idiopathic membranous nephropathy (IMN) is an antibody-mediated glomerulopathy in which podocyte-directed autoimmunity is well characterized, whereas the immunometabolic programs of innate immune cells within the renal microenvironment remain poorly defined. Src homology-2 domain-containing inositol 5-phosphatase 1 (SHIP1, encoded by Methods: Bulk and single-cell RNA-seq analyses were performed using public human IMN datasets, and the passive Heymann nephritis (PHN) rat model was used specifically for Results: IMN kidneys exhibited elevated immune and stromal scores, with increased infiltration of monocytes and naïve B cells and a relative depletion of regulatory T cells. Cross-differential analyses identified five overlapping immune-metabolic genes ( Conclusions: These data delineate an INPP5D/SHIP1-centered immunometabolic program in renal monocytes as a potential regulatory factor of pathological monocyte-podocyte crosstalk in IMN. Targeting SHIP1-related PI3K/Akt pathways and monocyte immunometabolism may offer novel immunomodulatory strategies for risk stratification and disease modification in membranous nephropathy.
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