Inflammatory Response Detection Service
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Patients with CKD exhibit a microinflammatory state characterized by elevated circulating inflammatory transmitters and changes in acute temporal protein levels due to decreased ability of the body to clear cytokines and metabolites, increased plasma endotoxin levels due to excessive volume loading, biocompatibility of dialysis membranes during hemodialysis treatment, contamination of dialysis fluid, infection of vascular access, and absorption of intestinal endotoxins due to weakened intestinal barrier during peritoneal dialysis treatment.
Regardless of the etiology, resident fibroblasts are key players in the pathogenesis of CKD and have been shown to play a critical role in the development and progression of the disease. In response to injury, resident fibroblasts transdifferentiate into myofibroblasts expressing α smooth muscle actin (αSMA) and have an increased capacity to produce large amounts of extracellular matrix (ECM) proteins, leading to renal fibrosis. During the myofibroblast transition described above, resident fibroblasts activate NF-κB signaling and produce pro-inflammatory cytokines and chemokines, thereby promoting inflammation. Furthermore, in the aging environment, resident fibroblasts transdifferentiate into several different phenotypes of fibroblasts, including CXCL13/CCL19-producing fibroblasts, retinoic acid-producing fibroblasts, and follicular dendritic cells in response to injury and orchestrate the formation of tertiary lymphoid tissue (TLT), which results in uncontrolled aberrant inflammation and impedes tissue repair.
Fibroblasts have two jobs during CKD: fibrosis and inflammation [1].
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