ArticleKidney international2010
Inhibition of integrin-linked kinase blocks podocyte epithelial-mesenchymal transition and ameliorates proteinuria.
Article in Kidney international, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.
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Who cites it
90 citing papers in PubMed, 148 citations in OpenAlex.
- A phase 1, single-dose study of fresolimumab, an anti-TGF-β antibody, in treatment-resistant primary focal segmental glomerulosclerosis.Kidney international · 2011Trial
- PTBP3 promotes diabetic nephropathy via Smad3-dependent podocyte-mesenchymal transition.Molecular biology reports · 2026Article
- Single-cell and high-resolution spatial profiling of podocytopathies reveals core mechanisms of podocyte injury.Science advances · 2026Article
- Biomimetic fractal topography enhances podocyte maturation in vitro.Nature communications · 2025Article
- Integrin Trafficking, Fibronectin Architecture, and Glomerular Injury upon Adiponectin Receptor 1 Depletion.Journal of the American Society of Nephrology : JASN · 2025Article
- Soluble Epoxide Hydrolase Inhibition Attenuates Proteinuria by Alleviating Renal Inflammation and Podocyte Injuries in Adriamycin-Induced Nephropathy.International journal of molecular sciences · 2024Article
- Role and Mechanisms of Tyro3 in Podocyte Biology and Glomerular Disease.Kidney diseases (Basel, Switzerland) · 2024Review
- Actin Cytoskeleton and Integrin Components Are Interdependent for Slit Diaphragm Maintenance inCells · 2024Article
- Evaluation of glomerular sirtuin-1 and claudin-1 in the pathophysiology of nondiabetic focal segmental glomerulosclerosis.Scientific reports · 2023Article
- Ulinastatin ameliorates podocyte ferroptosis via regulating miR-144-3p/SLC7A11 axis in acute kidney injury.In vitro cellular & developmental biology. Animal · 2023Article
- Mitofusin2 expression is associated with podocyte injury in IgA nephropathy.European journal of medical research · 2023Article
- Article
- Periostin as a Biomarker in the Setting of Glomerular Diseases-A Review of the Current Literature.Biomedicines · 2022Review
- Microtubule associated protein 4 phosphorylation-induced epithelial-to-mesenchymal transition of podocyte leads to proteinuria in diabetic nephropathy.Cell communication and signaling : CCS · 2022Article
- CXCL16/ERK1/2 pathway regulates human podocytes growth, migration, apoptosis and epithelial mesenchymal transition.Molecular medicine reports · 2022Article
- Partitioning defective 6 homolog alpha (PARD6A) promotes epithelial-mesenchymal transition via integrin β1-ILK-SNAIL1 pathway in ovarian cancer.Cell death & disease · 2022Article
- Pathogenic Role of MicroRNA Dysregulation in Podocytopathies.Frontiers in physiology · 2022Review
- Cellular phenotypic transitions in diabetic nephropathy: An update.Frontiers in pharmacology · 2022Review
- Profile of Podocyte Translatome During Development of Type 2 and Type 1 Diabetic Nephropathy Using Podocyte-Specific TRAP mRNA RNA-seq.Diabetes · 2021Article
- Tripterygium glycoside suppresses epithelial‑to‑mesenchymal transition of diabetic kidney disease podocytes by targeting autophagy through the mTOR/Twist1 pathway.Molecular medicine reports · 2021Article
30 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Proteinuria is a primary clinical symptom of a large number of glomerular diseases that progress to end-stage renal failure. Podocyte dysfunctions play a fundamental role in defective glomerular filtration in many common forms of proteinuric kidney disorders. Since binding of these cells to the basement membrane is mediated by integrins, we determined the role of integrin-linked kinase (ILK) in podocyte dysfunction and proteinuria. ILK expression was induced in mouse podocytes by various injurious stimuli known to cause proteinuria including TGF-beta1, adriamycin, puromycin, and high ambient glucose. Podocyte ILK was also found to be upregulated in human proteinuric glomerular diseases. Ectopic expression of ILK in podocytes decreased levels of the epithelial markers nephrin and ZO-1, induced mesenchymal markers such as desmin, fibronectin, matrix metalloproteinase-9 (MMP-9), and alpha-smooth muscle actin (alpha-SMA), promoted cell migration, and increased the paracellular albumin flux across podocyte monolayers. ILK also induced Snail, a key transcription factor mediating epithelial-mesenchymal transition (EMT). Blockade of ILK activity with a highly selective small molecule inhibitor reduced Snail induction and preserved podocyte phenotypes following TGF-beta1 or adriamycin stimulation. In vivo, this ILK inhibitor ameliorated albuminuria, repressed glomerular induction of MMP-9 and alpha-SMA, and preserved nephrin expression in murine adriamycin nephropathy. Our results show that upregulation of ILK is a convergent pathway leading to podocyte EMT, migration, and dysfunction. ILK may be an attractive target for therapeutic intervention of proteinuric kidney diseases.
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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.