ArticleApoptosis : an international journal on programmed cell death2024
IGFBP2 induces podocyte apoptosis promoted by mitochondrial damage via integrin α5/FAK in diabetic kidney disease.
Article in Apoptosis : an international journal on programmed cell death, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed.
- A protein-based prediction model for fragility fracture risk in individuals with diabetes.Journal of molecular cell biology · 2026Article
- Elucidating the therapeutic targets and multi-target mechanisms of salvianolic acid A for diabetic nephropathy.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Mitochondrial metabolic reprogramming drives diabetic kidney disease progression: cell-specific mechanisms, metabolic memory, and targeted strategies.Molecular medicine (Cambridge, Mass.) · 2026Review
- Urinary microenvironment-degradable nanocapsules for traceable therapy of diabetic nephropathy.Materials today. Bio · 2026Article
- Post‑translational modifications in diabetic kidney disease (Review).International journal of molecular medicine · 2026Review
- Chronic kidney disease onset, progression, and cardiovascular outcomes: proteomics informs biology and risk stratification.Cardiovascular diabetology · 2026Article
- From mechanisms to therapies: exploiting epigenetic and post-translational modifications of mitochondrial quality control in diabetic kidney disease.Frontiers in endocrinology · 2026Review
- IGFBP2 and IGFBP4 interact to activate complement pathway in diabetic kidney disease.Renal failure · 2025Article
- IGFBP5 promotes EndoMT and renal fibrosis through H3K18 lactylation in diabetic nephropathy.Cellular and molecular life sciences : CMLS · 2025Article
- Construction and evaluation of STZ-induced diabetes and diabetic kidney disease models in C57BL/6J mice.Frontiers in endocrinology · 2025Article
- Depletion of intrinsic renal macrophages with moderate-to-high expression ofTranslational andrology and urology · 2024Article
- Identification of Spatial Specific Lipid Metabolic Signatures in Long-Standing Diabetic Kidney Disease.Metabolites · 2024Article
- Podocyte Death in Diabetic Kidney Disease: Potential Molecular Mechanisms and Therapeutic Targets.International journal of molecular sciences · 2024Review
- Lithium-induced apoptotic cell death is not accompanied by a noticeable inflammatory response in the kidney.Frontiers in physiology · 2024Article
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Authors and funding
14 authors.
Funding
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Abstract
Podocyte apoptosis or loss is the pivotal pathological characteristic of diabetic kidney disease (DKD). Insulin-like growth factor-binding protein 2 (IGFBP2) have a proinflammatory and proapoptotic effect on diseases. Previous studies have shown that serum IGFBP2 level significantly increased in DKD patients, but the precise mechanisms remain unclear. Here, we found that IGFBP2 levels obviously increased under a diabetic state and high glucose stimuli. Deficiency of IGFBP2 attenuated the urine protein, renal pathological injury and glomeruli hypertrophy of DKD mice induced by STZ, and knockdown or deletion of IGFBP2 alleviated podocytes apoptosis induced by high concentration of glucose or in DKD mouse. Furthermore, IGFBP2 facilitated apoptosis, which was characterized by increase in inflammation and oxidative stress, by binding with integrin α5 (ITGA5) of podocytes, and then activating the phosphorylation of focal adhesion kinase (FAK)-mediated mitochondrial injury, including membrane potential decreasing, ROS production increasing. Moreover, ITGA5 knockdown or FAK inhibition attenuated the podocyte apoptosis caused by high glucose or IGFBP2 overexpression. Taken together, these findings unveiled the insight mechanism that IGFBP2 increased podocyte apoptosis by mitochondrial injury via ITGA5/FAK phosphorylation pathway in DKD progression, and provided the potential therapeutic strategies for diabetic kidney disease.
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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 Socratic graph.