ReviewClinical and experimental nephrology2014
Macrophage-mediated glucolipotoxicity via myeloid-related protein 8/toll-like receptor 4 signaling in diabetic nephropathy.
Review in Clinical and experimental nephrology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Cell apoptosis in ischemic stroke: Focus on lipid metabolism.Neural regeneration research · 2026Article
- A macrophage-endothelial cell axis in kidney diseases.International urology and nephrology · 2026Review
- Adipocyte death promotes hepatic infiltration of S100A8+ macrophages and steatotic liver disease progression in mice.The Journal of clinical investigation · 2025Article
- High-Density Lipoprotein in Patients with Diabetic Kidney Disease: Friend or Foe?International journal of molecular sciences · 2025Review
- Targeting lipid metabolic reprogramming to alleviate diabetic kidney disease: molecular insights and therapeutic strategies.Frontiers in immunology · 2025Review
- Asprosin Levels in Adults with Type 2 Diabetes Mellitus and Diabetic Kidney Disease: A Systematic Review and Meta-Analysis.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- Targeting Macrophages: Therapeutic Approaches in Diabetic Kidney Disease.International journal of molecular sciences · 2024Review
- Temporal alteration of serum bilirubin levels and its renoprotective effects in diabetic kidney disease: exploring the hormonal mechanisms.Frontiers in endocrinology · 2024Article
- Effects ofFrontiers in pharmacology · 2024Article
- Review
- Roles and crosstalks of macrophages in diabetic nephropathy.Frontiers in immunology · 2022Review
- Atherogenic dyslipidemia and diabetic nephropathy.Journal of nephrology · 2020Review
- Molecular hydrogen improves type 2 diabetes through inhibiting oxidative stress.Experimental and therapeutic medicine · 2020Article
- The predictive role of serum calprotectin on mortality in hemodialysis patients with high phosphoremia.BMC nephrology · 2020Observational
- Ablation of Myeloid Cell MRP8 Ameliorates Nephrotoxic Serum-induced Glomerulonephritis by Affecting Macrophage Characterization through Intraglomerular Crosstalk.Scientific reports · 2020Article
- Association of serum calprotectin (S100A8/A9) concentrations and idiopathic hyperlipidemia in Miniature Schnauzers.Journal of veterinary internal medicine · 2019Article
- Ageing potentiates diet-induced glucose intolerance, β-cell failure and tissue inflammation through TLR4.Scientific reports · 2018Article
- The Role of TLR4 on PGC-1Oxidative medicine and cellular longevity · 2018Article
- Nur77-deficiency in bone marrow-derived macrophages modulates inflammatory responses, extracellular matrix homeostasis, phagocytosis and tolerance.BMC genomics · 2016Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dyslipidemia is an independent risk factor for the development and progression of diabetic nephropathy (DN). In this review, we summarize mouse models with both diabetes and dyslipidemia, and their associated complications. We then discuss molecules potentially involved in deterioration of DN by dyslipidemia. We focus especially upon toll-like receptor 4 (TLR4) and one of its endogenous ligands, myeloid-related protein 8 (MRP8 or S100A8), since we have found that their mRNA levels are commonly increased in glomeruli of type 1 (streptozotocin [STZ]-induced) and type 2 (A-ZIP/F-1 lipoatrophic) diabetic mice. Gene expression of MRP8 and Tlr4 is further upregulated during worsening of STZ-induced DN by a high fat diet (HFD). Moreover, these HFD-induced changes are accompanied by enhanced gene expression of CCAAT element binding protein β and phosphorylation of c-Jun N-terminal kinase in the kidney, which have also been reported in pancreatic β cells under diabetic-hyperlipidemic conditions. Effects of a HFD upon DN are cancelled in Tlr4 knockout mice. Macrophages are the predominant source of MRP8 in glomeruli. In cultured macrophages, combinatorial treatment with high glucose and palmitate amplifies MRP8 expression in a Tlr4-dependent manner, and recombinant MRP8 protein markedly increases gene expression of the inflammatory cytokines interleukin-1β and tumor necrosis factor α. Here, we propose 'macrophage-mediated glucolipotoxicity' via activation of MRP8/TLR4 signaling as a novel mechanism of pathophysiology for DN.
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