ReviewDiabetes research and clinical practice2007
Novel roles of the IGF-IGFBP axis in etiopathophysiology of diabetic nephropathy.
Review in Diabetes research and clinical practice, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 59 citations in OpenAlex.
- Integrated bioinformatics and machine learning reveal pan-apoptosis and immune infiltration signatures in diabetic nephropathy.Frontiers in immunology · 2025Article
- Deciphering the multidimensional impact ofHeliyon · 2024Article
- Human umbilical cord mesenchymal stem cells attenuate diabetic nephropathy through the IGF1R-CHK2-p53 signalling axis in male rats with type 2 diabetes mellitus.Journal of Zhejiang University. Science. B · 2024Article
- The role and mechanism of action of miR-483-3p in mediating the effects of IGF-1 on human renal tubular epithelial cells induced by high glucose.Scientific reports · 2024Article
- Increased Levels of Circulating IGFBP4 and ANGPTL8 with a Prospective Role in Diabetic Nephropathy.International journal of molecular sciences · 2023Article
- IGFBP-6 Alters Mesenchymal Stromal Cell Phenotype Driving Dasatinib Resistance in Chronic Myeloid Leukemia.Life (Basel, Switzerland) · 2023Article
- A new ferritin SjFer0 affecting the growth and development of Schistosoma japonicum.Parasites & vectors · 2022Article
- Association of significantly elevated plasma levels of NGAL and IGFBP4 in patients with diabetic nephropathy.BMC nephrology · 2022Article
- Review
- IGFBP-1 expression is reduced in human type 2 diabetic glomeruli and modulates β1-integrin/FAK signalling in human podocytes.Diabetologia · 2021Article
- Investigation of the Mechanism of Complement System in Diabetic Nephropathy via Bioinformatics Analysis.Journal of diabetes research · 2021Article
- Novel Biomarkers in Patients with Chronic Kidney Disease: An Analysis of Patients Enrolled in the GCKD-Study.Journal of clinical medicine · 2020Article
- ROS- and HIF1α-dependent IGFBP3 upregulation blocks IGF1 survival signaling and thereby mediates high-glucose-induced cardiomyocyte apoptosis.Journal of cellular physiology · 2019Article
- ANGPTL4: A Predictive Marker for Diabetic Nephropathy.Journal of diabetes research · 2019Article
- Growth hormone (GH)-transgenic insulin-like growth factor 1 (IGF1)-deficient mice allow dissociation of excess GH and IGF1 effects on glomerular and tubular growth.Physiological reports · 2016Article
- Diabetic Retinopathy in Patients with Diabetic Nephropathy: Development and Progression.PloS one · 2016Article
- Podocytes, signaling pathways, and vascular factors in diabetic kidney disease.Advances in chronic kidney disease · 2014Review
- The molecular mechanism of rhein in diabetic nephropathy.Evidence-based complementary and alternative medicine : eCAM · 2014Review
- Mice deficient in PAPP-A show resistance to the development of diabetic nephropathy.The Journal of endocrinology · 2013Article
- Elevated IGFBP3 levels in diabetic tears: a negative regulator of IGF-1 signaling in the corneal epithelium.The ocular surface · 2012Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Mechanisms contributing to development of diabetic nephropathy (DN) remain unclear. High ambient glucose level transforms intracellular pathways, promoting stable phenotypic changes in the glomerulus such as mesangial cell hypertrophy, podocyte apoptosis, and matrix expansion. Insulin-like growth factors (IGFs) and the high affinity IGF binding proteins (IGFBPs) exert major effects on cell growth and metabolism. Compared with diabetic patients without microalbuminuria (MA), MA diabetic patients display perturbed GH-IGF-IGFBP homeostasis, including increased circulating IGF-I and IGFBP-3 protease activity, increased excretion of bioactive GH, IGF-I, and IGFBP-3, but decreased circulating IGFBP-3 levels. In diabetic animal models, expression of IGF-I and IGFBP-1 to -4 increases in key renal tissues and glomerular ulrafiltrate. Epithelial, mesangial, and endothelial cells derived from the kidney respond to IGF-I binding with increased protein synthesis, migration, and proliferation. This article reviews classic and emerging concepts for the roles of the GH-IGF-IGFBP axis in the etiopathophysiology, treatment, and prevention of diabetic renal disease. We report IGF-independent actions of IGFBP-3 in the podocyte for the first time.
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Registered trials
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.