ArticleDiabetologia2021
IGFBP-1 expression is reduced in human type 2 diabetic glomeruli and modulates β1-integrin/FAK signalling in human podocytes.
Article in Diabetologia, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- The insulin-like growth factor system and the progression of renal complications of type 2 diabetes.Diabetic medicine : a journal of the British Diabetic Association · 2026Article
- Exercise-induced cardiac hypertrophy: cellular and molecular mechanisms of cardiac adaptation following physical activity.Postepy w kardiologii interwencyjnej = Advances in interventional cardiology · 2026Review
- Immune Infiltration and Mitochondrial Function in Diabetic Kidney Disease: WGCNA and Machine Learning Identified Hub Genes with Clinical Validation.International journal of molecular sciences · 2026Article
- Chronic kidney disease onset, progression, and cardiovascular outcomes: proteomics informs biology and risk stratification.Cardiovascular diabetology · 2026Article
- Endothelial cell-released CD93 contributes to podocyte injury in idiopathic nephrotic syndrome.Science translational medicine · 2026Article
- A Functional Shift of IGFBP3 in Osteoarthritis: From Cartilage Protection to Disease Promotion.Journal of inflammation research · 2026Review
- Prioritization of potential drug targets for diabetic kidney disease using integrative omics data mining and causal inference.Journal of pharmaceutical analysis · 2025Article
- The role of IGFBP-1 in the clinical prognosis and pathophysiology of acute kidney injury.American journal of physiology. Renal physiology · 2025Observational
- Gonadal miRNomes and transcriptomes in infected fish reveal sexually dimorphic patterns of the immune response.Functional & integrative genomics · 2025Article
- Profiling of insulin-resistant kidney models and human biopsies reveals common and cell-type-specific mechanisms underpinning Diabetic Kidney Disease.Nature communications · 2024Article
- SIRPα modulates the podocyte cytoskeleton through influencing the phosphorylation of FAK at tyrosine residue 597.Acta biochimica et biophysica Sinica · 2024Article
- IGFBP2 induces podocyte apoptosis promoted by mitochondrial damage via integrin α5/FAK in diabetic kidney disease.Apoptosis : an international journal on programmed cell death · 2024Article
- STAT3-induced upregulation of lncRNA TTN-AS1 aggravates podocyte injury in diabetic nephropathy by promoting oxidative stress.Toxicology research · 2024Article
- Randomized Trial of SGLT2 Inhibitor Identifies Target Proteins in Diabetic Kidney Disease.Kidney international reports · 2024Article
- Identifying the Potential Diagnostic Gene Biomarkers and Forecasting the Potential Therapeutic Agents for Advanced Diabetic Nephropathy Based on Pyroptosis and Ferroptosis.Journal of inflammation research · 2024Article
- PFKFB3 downregulation aggravates Angiotensin II-induced podocyte detachment.Renal failure · 2023Article
- Signaling Pathways of the Insulin-like Growth Factor Binding Proteins.Endocrine reviews · 2023Article
- Identification and validation of immune and oxidative stress-related diagnostic markers for diabetic nephropathy by WGCNA and machine learning.Frontiers in immunology · 2023Article
- Identification of tubulointerstitial genes and ceRNA networks involved in diabetic nephropathy via integrated bioinformatics approaches.Hereditas · 2022Article
- Proteomics and Phosphoproteomics of Circulating Extracellular Vesicles Provide New Insights into Diabetes Pathobiology.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
20 authors at 4 institutions in 2 countries.
Funding
Abstract
aims/hypothesisPodocyte loss or injury is one of the earliest features observed in the pathogenesis of diabetic kidney disease (DKD), which is the leading cause of end-stage renal failure worldwide. Dysfunction in the IGF axis, including in IGF binding proteins (IGFBPs), is associated with DKD, particularly in the early stages of disease progression. The aim of this study was to investigate the potential roles of IGFBPs in the development of type 2 DKD, focusing on podocytes.
methodsIGFBP expression was analysed in the Pima DKD cohort, alongside data from the Nephroseq database, and in ex vivo human glomeruli. Conditionally immortalised human podocytes and glomerular endothelial cells were studied in vitro, where IGFBP-1 expression was analysed using quantitative PCR and ELISAs. Cell responses to IGFBPs were investigated using migration, cell survival and adhesion assays; electrical cell-substrate impedance sensing; western blotting; and high-content automated imaging.
resultsData from the Pima DKD cohort and from the Nephroseq database demonstrated a significant reduction in glomerular IGFBP-1 in the early stages of human type 2 DKD. In the glomerulus, IGFBP-1 was predominantly expressed in podocytes and controlled by phosphoinositide 3-kinase (PI3K)-forkhead box O1 (FoxO1) activity. In vitro, IGFBP-1 signalled to podocytes via β1-integrins, resulting in increased phosphorylation of focal-adhesion kinase (FAK), increasing podocyte motility, adhesion, electrical resistance across the adhesive cell layer and cell viability. CONCLUSIONS/
interpretationThis work identifies a novel role for IGFBP-1 in the regulation of podocyte function and that the glomerular expression of IGFBP-1 is reduced in the early stages of type 2 DKD, via reduced FoxO1 activity. Thus, we hypothesise that strategies to maintain glomerular IGFBP-1 levels may be beneficial in maintaining podocyte function early in DKD.
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