Fibrilácia predsiení (FP) je najčastejšia arytmia v klinickej praxi prispievajúca k zvýšenej morbidite a mortalite. Humorálne biomarkery, ako natriuretické peptidy, troponín, aldosterón, kortizol, kopeptín a apelín, zohrávajú čoraz dôležitejšiu úlo- hu v diagnostike, predikcii prognózy a manažmente FP. Zvýšené hladiny týchto biomarkerov naznačujú nielen poruchu funkcie myokardu a remodeláciu predsiení, ale aj zápalové a prokoagulačné stavy, ktoré ovplyvňujú vývoj a komplikácie FP. Sledovanie hladín biomarkerov poskytuje hlbší náhľad na patofyziologické mechanizmy FP a môže pomôcť pri identi- fikácii pacientov so zvýšeným rizikom komplikácií, ako sú tromboembolické príhody alebo progresia ochorenia. Integrácia biomarkerov do klinickej praxe môže výrazne zlepšiť stratifikáciu rizika, umožniť personalizovanejší prístup k liečbe FP a prispieť k efektívnejšiemu monitorovaniu priebehu ochorenia. Dôkazy o spojitosti medzi biomarkermi a FP sú povzbud- zujúce, avšak sú potrebné ďalšie štúdie na potvrdenie ich klinického využitia v štandardnej starostlivosti o pacientov s týmto závažným ochorením.
Atrial fibrillation (AF) is the most common arrhythmia in clinical practice, contributing to increased morbidity and mortality. Humoral biomarkers, such as natriuretic peptides, troponin, aldosterone, cortisol, copeptin, and apelin, are gaining importance in the diagnosis, prognosis, and management of AF. Elevated levels of these biomarkers indicate not only myocardial dysfunction and atrial remodeling but also inflammatory and procoagulant states that influence the progression and complications of AF. Monitoring biomarker levels provides deeper insight into the pathophysiological mechanisms of AF and can aid in identifying patients at higher risk of complications, such as thromboembolic events or disease progression. Integrating biomarkers into clinical practice can significantly improve risk stratification, facilitate a more personalized approach to AF treatment, and contribute to more effective disease monitoring. Evidence linking biomarkers with AF is promising; however, further studies are needed to confirm their clinical utility in standard care for patients with this serious condition.
- MeSH
- Aldosterone MeSH
- Apelin MeSH
- Arginine Vasopressin MeSH
- Biomarkers MeSH
- Atrial Fibrillation * diagnosis MeSH
- Hydrocortisone MeSH
- Humans MeSH
- Natriuretic Peptides MeSH
- Troponin blood MeSH
- Check Tag
- Humans MeSH
- Publication type
- Review MeSH
Polycystic ovary syndrome (PCOS) is associated with multiple risk factors for cardiovascular diseases, including insulin resistance, diabetes mellitus type 2, obesity, hypertension, and dyslipidaemia. Many studies have assessed the role of adipokines in the etiopathogenesis of PCOS, however, no single biomarker has been recognized to be in causal relation to the syndrome. Apelin has been identified as a new adipokine linked to obesity and insulin resistance. Some studies demonstrated that the apelin / apelin receptor could play a pivotal role in the pathogenesis of polycystic ovary syndrome, however the other yielded controversial results. Underlying mechanisms of possible involvement of apelin/apelin receptor complex are discussed.
- MeSH
- Adipokines MeSH
- Apelin MeSH
- Biomarkers MeSH
- Insulin Resistance * MeSH
- Humans MeSH
- Polycystic Ovary Syndrome * pathology MeSH
- Check Tag
- Humans MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
Apelin, the endogenous ligand of the G protein-coupled receptor (APJ), plays an important role in the physiological response to homeostatic perturbations. The aim of the present study was to investigate the effect of apelin on the functions of peritoneal macrophages. A double staining immunofluorescence technique was used to determine the expression of APJ in peritoneal macrophages. Rat peritoneal macrophages were randomly divided into three groups: control, apelin and apelin+F13A. A significant decrease in phagocytic and chemotactic activity of peritoneal macrophages resulted when the macrophages were incubated with [Pry(1)]-Apelin-13 (10 ng/ml). Incubation of peritoneal macrophages with the APJ receptor antagonist, F13A (20 ng/ml) prevented the suppressive effect of apelin on phagocytosis and chemotaxis. Peritoneal macrophages incubated with [Pry(1)]-Apelin-13 exhibited a decrease in the production of TNF-alpha and IL-6 compared to the control macrophages. Incubation of peritoneal macrophages with [Pry(1)]-Apelin-13 plus F13A prevented the decrease in the production of proinflammatory cytokines produced by [Pry(1)]-Apelin-13. In conclusion, apelin may be a mediator that inhibits the functions of activated macrophages.
- MeSH
- Apelin pharmacology MeSH
- Phagocytosis drug effects physiology MeSH
- Rats MeSH
- Inflammation Mediators metabolism MeSH
- Intercellular Signaling Peptides and Proteins pharmacology MeSH
- Macrophages, Peritoneal drug effects metabolism MeSH
- Rats, Wistar MeSH
- Cell Survival drug effects physiology MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
