ArticleCell death & disease2022
IGFBP5 promotes diabetic kidney disease progression by enhancing PFKFB3-mediated endothelial glycolysis.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers, 1 of them a synthesis that pooled it.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.
- The lactate-lactylation axis in renal fibrosis: potential mechanisms in diabetic kidney disease.Annals of medicine · 2025Pooled it
- miR-203 improves pressure overload-induced heart failure by targeting the IGFBP5/PI3K/AKT axis.Acta pharmacologica Sinica · 2026Article
- Article
- Lactate-Mediated Lysine Lactylation in Renal Fibrosis: Current Progress and Challenges.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Tubular PFKFB3 drives diabetic kidney fibrosis via lactate‑dependent H4K12 lactylation and HIPK2 transactivation.International journal of molecular medicine · 2026Article
- Mitochondrial metabolic reprogramming drives diabetic kidney disease progression: cell-specific mechanisms, metabolic memory, and targeted strategies.Molecular medicine (Cambridge, Mass.) · 2026Review
- Metabolic reprogramming in fibrosis-related diseases: underlying mechanisms and therapeutics.Molecular biomedicine · 2026Review
- IGFBP5 Restores Endometrial Receptivity and Rescues Implantation Failure in Polycystic Ovary Syndrome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Androgen receptor localisation and protein interactions provide insight into steroid mediated metabolic shifts in endocrine resistant breast cancer.NPJ breast cancer · 2026Article
- Lactylation: a metabolic-epigenetic bridge in diabetic kidney disease and a therapeutic target for TCM.Chinese medicine · 2026Review
- Anti-inflammatory effects of 3PO in asthmatic airway inflammation: an integrated study using network pharmacology, molecular modelling, andFrontiers in pharmacology · 2026Article
- Lactate Metabolism and Protein Lactylation in Diabetic Kidney Disease: A Narrative Review.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Role of metabolic reprogramming and lactylation in diabetic nephropathy: molecular mechanisms and therapeutic prospects - a narrative review.Frontiers in endocrinology · 2026Review
- New Insights into the Role of Mitochondrial Dysfunction in Diabetic Kidney Disease in the Omics Era.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- Multi-omics analysis identifies fibroblast IGFBP5 as a key target of anti-TNFα therapy in ulcerative colitis.Frontiers in immunology · 2026Article
- Metabolic reprogramming in diabetic complications: mechanisms, pathologies, and molecular evidence from multi-organ studies.Frontiers in immunology · 2026Review
- PFKFB3-Inhibitor 3PO-Mediated Glycolytic Reprogramming Promotes Inflammatory Dental Pulp Repair: An In Vitro and In Vivo Study.International endodontic journal · 2025Article
- IGFBP2 and IGFBP4 interact to activate complement pathway in diabetic kidney disease.Renal failure · 2025Article
- The new insights of lactate in various kidney diseases.Expert reviews in molecular medicine · 2025Review
- Activation of M1 macrophages promotes diabetic kidney disease by modulating glycolysis via HIF-1α-HK2 signaling pathway.Diabetology & metabolic syndrome · 2025Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Renal inflammation is a critical pathophysiological characteristic of diabetic kidney disease (DKD). The mechanism of the inflammatory response is complicated, and there are few effective treatments for renal inflammation that can be used clinically. Insulin-like growth factor-binding protein 5 (IGFBP5) is an important secretory protein that is related to inflammation and fibrosis in several tissues. Studies have shown that the IGFBP5 level is significantly upregulated in DKD. However, the function of IGFBP5 and its mechanism in DKD remain unclear. Here, we showed that IGFBP5 levels were significantly increased in the kidneys of diabetic mice. Ablation of IGFBP5 alleviated kidney inflammation in DKD mice. Mechanistically, IGFBP5 increased glycolysis, which was characterized by increases in lactic acid and the extracellular acidification rate, by activating the transcription factor early growth response 1 (EGR1) and enhancing the expression of PFKFB3 in endothelial cells. Furthermore, a mutation in PFKFB3 attenuated renal inflammation in DKD mice. Taken together, we provided evidence that IGFBP5 enhanced kidney inflammation through metabolic reprogramming of glomerular endothelial cells. Our results provide new mechanistic insights into the effect of IGFBP5 on kidney and highlight potential therapeutic opportunities for IGFBP5 and the metabolic regulators involved in DKD.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.