ArticleMolecular metabolism2019
Tim-3 aggravates podocyte injury in diabetic nephropathy by promoting macrophage activation via the NF-κB/TNF-α pathway.
Article in Molecular metabolism, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 111 papers, 2 of them syntheses that pooled it.
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Who cites it
111 citing papers in PubMed, 2 syntheses or guidelines pooled it, 183 citations in OpenAlex.
- Mechanism of Ganoderma lucidum polysaccharides in the mangement of diabetes and its complications.Frontiers in pharmacology · 2026Pooled it
- An Emerging Role of TIM3 Expression on T Cells in Chronic Kidney Inflammation.Frontiers in immunology · 2021Pooled it
- Bibliometric analysis of SGLT2 inhibitor treatment for diabetic kidney disease.Renal failure · 2026Review
- Gegen Flavonoids and Huangqi Saponins Combination Ameliorates Diabetic Nephropathy By Modulating the Gut-Kidney Axis and Regulating Macrophage Polarization.Applied biochemistry and biotechnology · 2026Article
- Renal Tubular Epithelial CRLF1 Interacts With ITGB1 to Accelerate Fibrosis During the Transition From AKI to CKD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- ZDHHC8-mediated S-palmitoylation of RAD21 causes mitochondrial dysfunction in diabetic nephropathy via inhibiting ACSM3 transcription.Cell death and differentiation · 2026Article
- Unlocking the roles of plasma soluble T-cell immunoglobulin and mucin domain-containing protein 3 in kidney diseases: findings from native and allograft biopsy cohorts.Molecular biomedicine · 2026Article
- Integration of multi-omics and network toxicology reveals TLR4-mediated nephrotoxicity induced by arecoline.BMC pharmacology & toxicology · 2026Article
- TIM-3 in Cardiovascular Disease.Current heart failure reports · 2026Review
- Linderalactone mitigates diabetic renal injury by inhibiting macrophage inflammation via the Dectin1/Syk/CARD9/IRF5/NF-κB pathway.Journal of diabetes investigation · 2026Article
- Immune checkpoint TIM-3 in tumor immunotherapy.Acta biochimica et biophysica Sinica · 2026Review
- TIM-3+ Macrophages: Insights into Their Role in Cancer and Inflammation.International journal of molecular sciences · 2026Review
- CD4Frontiers in immunology · 2026Review
- Exosomal regulation of cellular reprogramming and polarization in the tumor microenvironment.Cancer cell international · 2025Review
- The relationship between periodontitis and proteinuria in chronic kidney disease: A review.Medicina oral, patologia oral y cirugia bucal · 2025Review
- Activation of M1 macrophages promotes diabetic kidney disease by modulating glycolysis via HIF-1α-HK2 signaling pathway.Diabetology & metabolic syndrome · 2025Article
- Effects of dapagliflozin on podocyte damage and oxidative stress in patients with diabetic nephropathy.Diabetology & metabolic syndrome · 2025Article
- Targeting to Intensify M2 Macrophage Polarization Ameliorate Podocyte Lipid Accumulation and Damage by Tea Polyphenols via Activating SIRT1 in the Aged Model Rats With DKD.Food science & nutrition · 2025Article
- hucMSC-derived exosomes targeting macrophage polarization attenuate systemic inflammation in T1DM via INS/SOD1 delivery.Stem cell research & therapy · 2025Article
- The role of Tim-3+T cell subsets in the peripheral blood of patients with COVID-19 and diabetes.iScience · 2025Article
51 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveMacrophage-mediated inflammation plays a significant role in the development and progression of diabetic nephropathy (DN). However, the underlying mechanisms remain unclear. Studies suggest that T cell immunoglobulin domain and mucin domain-3 (Tim-3) has complicated roles in regulating macrophage activation, but its roles in the progression of DN are still completely unknown.
methodsWe downregulated Tim-3 expression in kidney (intrarenal injection of Tim-3 shRNA expressing lentivirus or global Tim-3 knockout mice) and induced DN by streptozotocin (STZ). We analyzed the degree of renal injury, especially the podocyte injury induced by activated macrophages in vitro and in vivo. Then, we transferred different bone marrow derived macrophages (BMs) into STZ-induced Tim-3 knockdown mice to examine the effects of Tim-3 on macrophages in DN.
resultsFirst, we found that Tim-3 expression on renal macrophages was increased in patients with DN and in two diabetic mouse models, i.e. STZ-induced diabetic mice and db/db mice, and positively correlated with renal dysfunction of DN patients. Tim-3 deficiency ameliorated renal damage in STZ-induced diabetes with concurrent increase in protein levels of Nephrin and WT-1. Similar effects were observed in mice with Tim-3 knockdown diabetic mice. Second, adoptive transfer of Tim-3-expressing macrophages, but not Tim-3 knockout macrophages, accelerated diabetic renal injury in DN mice, suggesting a key role for Tim-3 on macrophages in the development of DN. Furthermore, we found NF-κB activation and TNF-α excretion were upregulated by Tim-3 in diabetic kidneys, and podocyte injury was associated with the Tim-3-mediated activation of the NF-κB/TNF-α signaling pathway in DN macrophages both in vivo and in vitro.
conclusionsThese results suggest that Tim-3 functions as a key regulator in renal inflammatory processes and serves as a potential therapeutic target for renal injury in DN.
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