Biological variation of established and novel biomarkers for atherosclerosis: Results from a prospective, parallel-group cohort study

Functional and transcriptomic analysis of extracellular vesicles identifies calprotectin as a new prognostic marker in peripheral arterial disease (PAD)

“…We determined calprotectin levels in the serum of patients included in the transcriptomic analysis and observed a linear association with S100A9 mRNA, encouraging its analysis in the expanded control and PAD populations. As previously described [45], we found increased levels of calprotectin in PAD samples, even though our control subjects were older and had at least two known cardiovascular risk factors. No significant differences were observed, however, when assessing its diagnostic potential.…”

“…Calprotectin (S100A8/A9) was selected for validation according to the relative abundance of S100A9 transcript in the RNA‐Seq data. Moreover, it has shown associations with plaque instability [41,42] and cardiovascular complications in the general population [43] and in patients with acute coronary syndromes [44], while its role in PAD has been scarcely studied [45]. We determined calprotectin levels in the serum of patients included in the transcriptomic analysis and observed a linear association with S100A9 mRNA, encouraging its analysis in the expanded control and PAD populations.…”

Human β-defensin 3 suppresses Porphyromonas gingivalis lipopolysaccharide-induced inflammation in RAW 264.7 cells and aortas of ApoE-deficient mice

“…In our experiment, endothelial dysfunction of ApoE-deficient mice resulted from chronic exposure to Pg-LPS was marked by the up-regulation of ICAM-1, VCAM-1, and circulated sICAM-1. Indeed, many inflammatory agents serve as biomarkers in coronary artery disease, for instance, increased levels of MCP-1 and sICAM-1 are also early markers for preclinical atherosclerosis [6,37].…”

Pathomorphism of Limb Major Vessels in Experimental Atherogenic Inflammation. The Role of Adventitial Intimal Relations (Review)

“…Thus, the diagnostics of separate markers in atherogenic inflammation analysis is confined by nature to form a strategy for controlling atherogenesis [38]. Current strategy in atherogenic inflammation study with a view to advanced technologies of making drug and medical products aimed at indirect and direct effective control of molecule-cell-tissue structures of vascular walls with early atheromatosis requires revealing fine reconstruction mechanisms.…”

“…Impaired expression balance of pro-atherogenic (proinflammatory) and anti-atherogenic (anti-inflammatory) cell markers if hyperlipidemia conditions are preserved stabilize destruction in subendothelial space. The expression of blood residual cell receptors under vascular endothelium and of vascular endothelium itself, namely: endothelin-1 [31][32][33][34][35], caveolins-1, -2, and -3 [36, 37], selectins Р (CD62P), Е (CD62E), L (CD62L), and antibodies to them on vascular endothelium, lymphocytes and platelets [38][39][40], intercellular adhesion molecule-1 (ICAM-1) marker [41][42][43], vascular cell adhesion molecule-1 (VCAM-1) marker [44][45][46][47], monocyte chemotactic protein (MCP-1) [48][49][50], macrophage colony-stimulating factor (MCSF) [51][52][53][54][55][56][57], pleiotropic cytokine (TNF-α) [58][59][60][61][62][63][64], С-reactive protein (CRP) [65][66][67][68][69][70], platelet derived growth factor (PDGF) [71][72][73][74][75][76][77], interleukin family in atherosclerosis <...>…”