Authors: Z. Guľašová 1; Z. Hertelyová 1; D. Szabóová 1,2; V. Tomečková 3 Authors‘ workplace: Centrum klinického a predklinického výskumu, MEDIPARK, Lekárska fakulta UPJŠ v Košiciach 1; Ústav patologickej fyziológie, Lekárska fakulta UPJŠ v Košiciach 2; Ústav lekárskej a klinickej biochémie, Lekárska fakulta UPJŠ v Košiciach 3 Published in: Klin. Biochem. Metab., 34, 2026, No. 1, p. 26-29 doi: https://doi.org/10.61568/kbm.2026.005
Endothelial dysfunction is considered an early marker of atherosclerosis. Vascular calcification is highly prevalent in patients with ischemic cardiovascular disease, cerebrovascular disorder, and renal failure, being a common feature in aging, diabetes, dyslipidemia, abnormal valve biomechanics, end-stage renal disease, and atherosclerosis, a major cause of mortality and morbidity. Oxidative stress promotes calcification of vascular smooth muscle cells (SMC) by increasing the expression and activity of osteogenic transcription factors in atherosclerotic plaques. SMC expresses various markers of osteogenic differentiation in calcified atherosclerotic lesions. Interestingly, decreased levels of some bone factors accelerate vascular calcification and injured tissue regeneration. Another key player in endothelial remodeling is amino acid metabolism. Branched-chain amino acids are catabolized in several non-hepatic tissues, including cardiac muscle. Immune activation and inflammation in patients with cardiovascular disease are associated with higher phenylalanine-to-tyrosine ratios.
Amino acid metabolism – vascular calcification – endothelial remodeling
Don‘t have an account? Create new account
Enter the email address that you registered with. We will send you instructions on how to set a new password.
