ArticleFrontiers in immunology2022
Excessive Activation of Notch Signaling in Macrophages Promote Kidney Inflammation, Fibrosis, and Necroptosis.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 85 papers, 1 of them a synthesis that pooled it.
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Who cites it
85 citing papers in PubMed, 1 synthesis or guideline pooled it, 103 citations in OpenAlex.
- Macrophages in Renal Injury, Repair, Fibrosis Following Acute Kidney Injury and Targeted Therapy.Frontiers in immunology · 2022Pooled it
- Acute renal injury in ANCA-associated glomerulonephritis: etiology related to acute tubulointerstitial injury versus glomerular injury.Renal failure · 2026Article
- KLF transcription factors in metabolic kidney disease: from podocyte protection to tubulointerstitial fibrosis.International urology and nephrology · 2026Review
- Characterizing the Immune Cell Infiltration in Renal Interstitium and Therapeutic Targets of Drugs in Diabetic Nephropathy by Multiomics Study.Diabetes & metabolism journal · 2026Article
- Review
- Zhenwu Decoction Alleviates Renal Fibrosis by Disrupting the Bidirectional Crosstalk Between TGF-β/Smad and Notch Signaling.Journal of cellular physiology · 2026Article
- Engineering Oncolytic Virus-Armed Macrophages for Enhanced Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Programmed cell death and metastatic evolution in breast cancer: the role of anoikis, necroptosis, and ferroptosis.Apoptosis : an international journal on programmed cell death · 2026Review
- Exosomal lncRNA OTUD6B-AS1 as a pathogenic nanocarrier promotes inflammatory macrophage polarization in endometritis via a targetable ceRNA circuit.Materials today. Bio · 2026Article
- Identification and regulatory mechanism analysis of macrophage-related key genes in diabetic nephropathy.Diabetology & metabolic syndrome · 2026Article
- Necroptosis induced by MLKL overexpression in liver triggers cellular senescence and leads to chronic inflammation and fibrosis.GeroScience · 2026Article
- Molecular Mechanisms and Clinical Evidence Supporting the Four Pillars of Therapy in Diabetic Kidney Disease: Emerging Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- LYVE1 ectodomain shedding blunts lymphatic transmigration and clearance of macrophages during kidney injury.JCI insight · 2026Article
- Metabolic syndrome necroptosis: disease implications and therapeutic targeting.Journal of physiology and biochemistry · 2026Review
- Inflammation and Diabetic Kidney Disease.International journal of molecular sciences · 2026Review
- Asiatic Acid AttenuatesInternational journal of molecular sciences · 2026Article
- Metabolic Reprogramming and Immunometabolic Dysregulation in Diabetic Kidney Disease: From Pathogenesis to Precision Multi-target Therapies.Research (Washington, D.C.) · 2026Review
- Shenlian (SL) Decoction Treat Diabetic Nephropathy by Regulating M1 Polarization of Macrophages and Pyroptosis of Renal Tubular Epithelial Cells.Journal of diabetes research · 2026Article
- Tubular injury in diabetic kidney disease: a focus on regulated cell death.Frontiers in endocrinology · 2026Review
- COL1A2 and APOLD1 Define a Dual-Axis Molecular Framework for Diabetic Nephropathy-Retinopathy Comorbidity: An Integrative Multiomics and Machine Learning Study in Mouse Models.International journal of medical sciences · 2026Article
25 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Diabetic nephropathy (DN) is one of the main causes of end-stage renal disease (ESRD). Existing treatments cannot control the progression of diabetic nephropathy very well. In diabetic nephropathy, Many monocytes and macrophages infiltrate kidney tissue. However, the role of these cells in the pathogenesis of diabetic nephropathy has not been fully elucidated. In this study, we analyzed patient kidney biopsy specimens, diabetic nephropathy model animals. Meanwhile, we cocultured cells and found that in diabetic nephropathy, damaged intrinsic renal cells (glomerular mesangial cells and renal tubular epithelial cells) recruited monocytes/macrophages to the area of tissue damage to defend against and clear cell damage. This process often involved the activation of different types of macrophages. Interestingly, the infiltrating macrophages were mainly M1 (CD68+iNOS+) macrophages. In diabetic nephropathy, crosstalk between the Notch pathway and NF-κB signaling in macrophages contributed to the polarization of macrophages. Hyperpolarized macrophages secreted large amounts of inflammatory cytokines and exacerbated the inflammatory response, extracellular matrix secretion, fibrosis, and necroptosis of intrinsic kidney cells. Additionally, macrophage depletion therapy with clodronate liposomes and inhibition of the Notch pathway in macrophages alleviated the pathological changes in kidney cells. This study provides new information regarding diabetic nephropathy-related renal inflammation, the causes of macrophage polarization, and therapeutic targets for diabetic nephropathy.
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