Search for: [Abstract = "Background Aortic stenosis \(AS\) is the most common cause of acquired valvular heart disease in individuals over 65 years of age, with no available pharmacological treatment. The pathomechanism of AS is a complex and tightly regulated process involving the activation of multiple molecular, cellular, and tissue pathways. Numerous studies indicate that elevated levels of lipoproteins, oxidized phospholipids \(OxPL\), or coexisting type 2 diabetes \(DMT2\) may accelerate the development of AS. However, the underlying mechanisms by which these factors influence inflammation, coagulation and fibrinolysis pathways, and aortic valve calcification have not been fully elucidated. Aims To investigate the mechanisms involving factors favouring AS progression, such as hyperglycemia and increased oxidative stress, with particular emphasis on their potential associations with inflammation, coagulation activation, hypofibrinolysis, and calcification in patients with severe AS. Methods and Results In Publication 1, 76 patients with severe AS \(without DMT2\) and 50 patients with AS and DMT2 \(AS\-DM\) were studied. Valvular expression of advanced glycation end products \(AGEs\) and receptor for AGEs \(RAGE\) was evaluated by immunofluorescence. Levels of AGEs and soluble isoform of RAGE \(sRAGE\) in serum were assessed using ELISA tests. AS\-DM patients exhibited increased accumulation of AGEs and RAGE wi"]

Number of results: 1