ArticleExperimental & molecular medicine2022
Indoxyl sulfate- and P-cresol-induced monocyte adhesion and migration is mediated by integrin-linked kinase-dependent podosome formation.
Article in Experimental & molecular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 25 citations in OpenAlex.
- Elevated microbially-derived metabolites in autism: a possible diagnostic screening test for a distinct ASD phenotype.Molecular psychiatry · 2026Article
- ILK-Dependent Modulation of DPP4 Prevents Progression of Calcific Aortic Valve Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- ILK Deletion Protects Against Chronic Kidney Disease-Associated Vascular Damage.International journal of molecular sciences · 2025Article
- Elevated Microbially-Derived Metabolites in Autism: A Possible Diagnostic Screening Test for a Distinct ASD Phenotype.Research square · 2025Article
- Microphysiological Uremia Model Reveals Biophysical Potentiators of Vascular Dysfunction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Spatial metabolic and phenotypic characterization of the germ-free mouse model.Annals of the New York Academy of Sciences · 2025Article
- Gamma-tocopherol vitamin E enhances the cytotoxicity of p-cresyl sulfate to renal tubular cells.European journal of medical research · 2025Article
- Integrin-Linked Kinase (ILK) Promotes Mitochondrial Dysfunction by Decreasing CPT1A Expression in a Folic Acid-Based Model of Kidney Disease.International journal of molecular sciences · 2025Article
- Vascular inflammation in chronic kidney disease: the role of uremic toxins in macrophage activation.Frontiers in cardiovascular medicine · 2025Review
- UnravelingFrontiers in pharmacology · 2025Review
- Interleukin-6 as a Director of Immunological Events and Tissue Regenerative Capacity in Hemodialyzed Diabetes Patients.Medical sciences (Basel, Switzerland) · 2024Article
- Indoxyl Sulfate-Induced Macrophage Toxicity and Therapeutic Strategies in Uremic Atherosclerosis.Toxins · 2024Review
- Integrin-linked kinase mRNA expression in circulating mononuclear cells as a biomarker of kidney and vascular damage in experimental chronic kidney disease.Cell communication and signaling : CCS · 2024Article
- ILK inhibition reduces osteophyte formation through suppression of osteogenesis in BMSCs via Akt/GSK-3β/β-catenin pathway.Molecular biology reports · 2024Article
- The gut microbiome tango in the progression of chronic kidney disease and potential therapeutic strategies.Journal of translational medicine · 2023Review
- Uremic Toxins Induce THP-1 Monocyte Endothelial Adhesion and Migration through Specific miRNA Expression.International journal of molecular sciences · 2023Article
- Mesenchymal Migration on Adhesive-Nonadhesive Alternate Surfaces in Macrophages.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- The Molecular Mechanism and Therapeutic Strategy of Cardiorenal Syndrome Type 3.Reviews in cardiovascular medicine · 2023Review
- Immune System Dysfunction and Inflammation in Hemodialysis Patients: Two Sides of the Same Coin.Journal of clinical medicine · 2022Review
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
Abstract
Cardiovascular disease is an important cause of death in patients with chronic kidney disease (CKD). Protein-bound uremic toxins, such as p-cresyl and indoxyl sulfate (IS), are poorly removed during hemodialysis, leading to vascular endothelial dysfunction and leukocyte extravasation. These processes can be related to dynamic adhesion structures called podosomes. Several studies have indicated the role of integrin-linked kinase (ILK) in the accumulation of integrin-associated proteins in podosomes. Here, we investigated the involvement of ILK and podosome formation in the adhesion and extravasation of monocytes under p-cresol (pc) and IS exposure. Incubation of THP-1 human monocyte cells with these toxins upregulated ILK kinase activity. Together, both toxins increased cell adhesion, podosome formation, extracellular matrix degradation, and migration of THP-1 cells, whereas ILK depletion with specific small interfering RNAs suppressed these processes. Interestingly, F-actin colocalized with cortactin in podosome cores, while ILK was colocalized in podosome rings under toxin stimulation. Podosome Wiskott-Aldrich syndrome protein (WASP)-interacting protein (WIP) and AKT protein depletion demonstrated that monocyte adhesion depends on podosome formation and that the ILK/AKT signaling pathway is involved in these processes. Ex vivo experiments showed that both toxins induced adhesion and podosome formation in leukocytes from wild-type mice, whereas these effects were not observed in leukocytes of conditional ILK-knockdown animals. In summary, under pc and IS stimulation, monocytes increase podosome formation and transmigratory capacity through an ILK/AKT signaling pathway-dependent mechanism, which could lead to vascular injury. Therefore, ILK could be a potential therapeutic target for the treatment of vascular damage associated with CKD.
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