ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2020
TAB1 regulates glycolysis and activation of macrophages in diabetic nephropathy.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 70 citations in OpenAlex.
- Hypoxia-inducible factor-1 (HIF-1) in the molecular mechanisms of liver fibrosis: research progress on its role and therapeutic strategies.Journal of applied genetics · 2026Review
- Therapeutic Regulation of Macrophage Polarization for Diabetic Kidney Disease by Targeted Metabolic Reprogramming.Current medical science · 2026Review
- Natural Products Modulate Plaque Macrophage Functional Programs in Atherosclerosis.Drug design, development and therapy · 2026Review
- Berberine Ameliorates Diabetic Kidney Disease by Modulating Macrophage Polarization via Inhibiting IL-17A Signaling.Journal of inflammation research · 2026Article
- Metabolic reprogramming in diabetic complications: mechanisms, pathologies, and molecular evidence from multi-organ studies.Frontiers in immunology · 2026Review
- Macrophage polarization in diabetic vascular complications: mechanistic insights and therapeutic targets.Journal of translational medicine · 2025Review
- Qi-Gui-Sheng-Jiang-San Decoction Regulating Hypoxia Response Through Non-Oxygen-Dependent Pathway Improves Diabetic Kidney Disease: Coupling Network Pharmacology With Experimental Verification.Journal of diabetes research · 2025Article
- HIF-1-mediated macrophage metabolic reprogramming promotes AKI to CKD transition.International journal of biological sciences · 2025Article
- ITGAM-mediated macrophages contribute to basement membrane damage in diabetic nephropathy and atherosclerosis.BMC nephrology · 2024Article
- Down-regulated TAB1 suppresses the replication of Coxsackievirus B5 via activating the NF-κB pathways through interaction with viral 3D polymerase.Virology journal · 2023Article
- Cellular crosstalk of mesangial cells and tubular epithelial cells in diabetic kidney disease.Cell communication and signaling : CCS · 2023Review
- Article
- The impact of hypoxia-inducible factors in the pathogenesis of kidney diseases: a link through cell metabolism.Kidney research and clinical practice · 2023Article
- Effects of glycolysis on the polarization and function of tumor‑associated macrophages (Review).International journal of oncology · 2023Review
- Integrated analysis of RNA methylation regulators crosstalk and immune infiltration for predictive and personalized therapy of diabetic nephropathy.Human genomics · 2023Article
- Targeting immunometabolism during cardiorenal injury: roles of conventional and alternative macrophage metabolic fuels.Frontiers in physiology · 2023Review
- Kirenol alleviates diabetic nephropathy via regulating TGF-β/Smads and the NF-κB signal pathway.Pharmaceutical biology · 2022Article
- The Role of Hypoxia-Inducible Factor-1 Alpha in Renal Disease.Molecules (Basel, Switzerland) · 2022Review
- Metabolic signatures of immune cells in chronic kidney disease.Expert reviews in molecular medicine · 2022Review
- Tubular epithelial cell-derived extracellular vesicles induce macrophage glycolysis by stabilizing HIF-1α in diabetic kidney disease.Molecular medicine (Cambridge, Mass.) · 2022Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
OBJECTIVE AND
designMacrophages exhibit strong phenotypic plasticity and can mediate renal inflammation by polarizing into an M1 phenotype. They play a pivotal role in diabetic nephropathy (DN). Here, we have investigated the regulatory role of transforming growth factor β-activated kinase 1-binding protein 1 (TAB1) in glycolysis and activation of macrophages during DN.
methodsTAB1 was inhibited using siRNA in high glucose (HG)-stimulated bone marrow-derived macrophages (BMMs) and lentiviral vector-mediated TAB1 knockdown was used in streptozotocin (STZ)-induced diabetic mice. Western blotting, flow cytometry, qRT-PCR, ELISA, PAS staining and immunohistochemical staining were used for assessment of TAB1/nuclear factor-κB (NF-κB)/hypoxia-inducible factor-1α (HIF-1α), iNOS, glycolysis, inflammation and the clinical and pathological manifestations of diabetic nephropathy.
resultsWe found that TAB1/NF-κB/HIF-1α, iNOS and glycolysis were up-regulated in BMMs under HG conditions, leading to release of further inflammatory factors, Downregulation of TAB1 could inhibit glycolysis/polarization of macrophages and inflammation in vivo and in vitro. Furthermore, albuminuria, the tubulointerstitial damage index and glomerular mesangial expansion index of STZ-induced diabetic nephropathy mice were decreased by TAB1 knockdown.
conclusionsOur results suggest that the TAB1/NF-κB/HIF-1α signaling pathway regulates glycolysis and activation of macrophages in DN.
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