Impact of Uremic Toxins on Endothelial Dysfunction in Chronic Kidney Disease
| Jazyk: | angličtina |
|---|---|
| Rok vydání: | 2022 |
| Předmět: |
Cardiovascular Diseases/complications
DOWN-REGULATION vascular pathophysiology P-CRESYL SULFATE SMOOTH-MUSCLE-CELLS uremic toxins Apoptosis Chronic/diagnosis endothelial dysfunction ENDOPLASMIC-RETICULUM STRESS cardiovascular disease VASCULAR CALCIFICATION PROTEIN CARBAMYLATION Animals Humans Endothelium Renal Insufficiency OXIDATIVE STRESS Protein Processing Endothelial Cells/drug effects Post-Translational Vascular/metabolism Uremic Toxins/adverse effects vascular dysfunction Endoplasmic Reticulum Stress endothelial cells LOW-DENSITY LIPOPROTEINS CARDIOVASCULAR-DISEASE Nitric Oxide/metabolism Disease Susceptibility GLYCATION END-PRODUCTS Biomarkers chronic kidney disease Signal Transduction |
| Zdroj: | International Journal of Molecular Sciences. 23(1) |
| ISSN: | 1422-0067 1661-6596 |
| Popis: | Patients with chronic kidney disease (CKD) are at a highly increased risk of cardiovascular complications, with increased vascular inflammation, accelerated atherogenesis and enhanced thrombotic risk. Considering the central role of the endothelium in protecting from atherogenesis and thrombosis, as well as its cardioprotective role in regulating vasorelaxation, this study aimed to systematically integrate literature on CKD-associated endothelial dysfunction, including the underlying molecular mechanisms, into a comprehensive overview. Therefore, we conducted a systematic review of literature describing uremic serum or uremic toxin-induced vascular dysfunction with a special focus on the endothelium. This revealed 39 studies analyzing the effects of uremic serum or the uremic toxins indoxyl sulfate, cyanate, modified LDL, the advanced glycation end products N-carboxymethyl-lysine and N-carboxyethyl-lysine, p-cresol and p-cresyl sulfate, phosphate, uric acid and asymmetric dimethylarginine. Most studies described an increase in inflammation, oxidative stress, leukocyte migration and adhesion, cell death and a thrombotic phenotype upon uremic conditions or uremic toxin treatment of endothelial cells. Cellular signaling pathways that were frequently activated included the ROS, MAPK/NF-κB, the Aryl-Hydrocarbon-Receptor and RAGE pathways. Overall, this review provides detailed insights into pathophysiological and molecular mechanisms underlying endothelial dysfunction in CKD. Targeting these pathways may provide new therapeutic strategies reducing increased the cardiovascular risk in CKD. |
| Databáze: | OpenAIRE |
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