Myeloperoxidase (MPO), a heme protein released by leukocytes, is one of the most widely studied during the last decades molecule that plays a crucial role in inflammation and oxidative stress in the cellular level. It has become increasingly recognized that MPO performs a very important role as part of the innate immune system through the formation of microbicidal reactive oxidants, whilst it affects the arterial endothelium with a number of mechanisms that include modification of net cellular cholesterol flux and impairment of Nitric Oxide (NO)-induced vascular relaxation. In that way, MPO is implicated into both the formation and propagation of atheromatosis and there is substantial evidence that it also promotes ischemia through destabilization of the vulnerable plaque. Numerous studies have added information on the notion that MPO and its oxidant products are part of the inflammatory cascade initiated by endothelial injury and they are significantly overproduced at the site of arterial inflammation. Subsequent studies achieved quantification of this observation showing significant elevations of the systemic levels of MPO in a wide spectrum of cardiovascular disease scenarios with acute coronary syndromes and heart failure being the most studied. This review highlights key-aspects of MPO's pathophysiological properties and summarizes the role of MPO as a diagnostic and prognostic tool for a number of cardiovascular pathologies.
Asymmetric Dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) production. ADMA is generated from methylation of arginine residues by protein arginine methyltransferases (PRMTs) and subsequent proteolysis, while its elimination is achieved mainly by degradation with dimethylarginine dimethylaminohydrolase (DDAH). Oxidative stress, endothelial nitric oxide synthase (eNOS) inhibition, eNOS uncoupling, inflammation and shear stress play a pivotal role in ADMA pathophysiology by managing PRMT/DDAH expression and NO synthesis and leading to a common result - endothelial dysfunction. Endothelial dysfunction seems to be the common finding in studies investigating the role of ADMA in cardiovascular disease (CVD). High-performance liquid chromatography (HPLC), mass spectrometry (MS) and enzyme-linked immunosorbent assay (ELISA) are the existing methods for ADMA quantification. However, none of them fulfils all the criteria to be characterized as "gold standard". ADMA is significantly associated with risk factors for CVD and almost with every disease of the cardiovascular system; showing an independent, strong prognostic value for mortality and future cardiovascular events. This article aims to review the current knowledge about ADMA biology and metabolism, pathophysiological mechanisms implicating ADMA in CVD, methods for the determination of ADMA and its association with CVD risk factors and established CVDs.
Essential hypertension is a common health disorder with uncertain etiology and unclear pathophysiology. There is evidence that various systems interact in uncertain ways and mechanisms to cause hypertension. It is also well known that inflammation is a key feature in the initiation, progression and clinical implication of several cardiovascular diseases. Recently, it has become evident that the immune system and inflammatory response are also essential in the pathogenesis of hypertension. Many inflammation markers such as CRP, cytokines, and adhesion molecules have been found elevated in hypertensive patients supporting the role of inflammation in the pathogenesis of hypertension. Also, in normotensive individuals, these markers have been associated with the risk of developing hypertension, whereas in hypertensive patients they have been associated with target organ damage as well as with the risk for future cardiovascular events. Thus, understanding the role of inflammation in hypertension provides new insights for novel therapeutic approaches, targeting inflammation for the treatment of hypertension and its complications.
Cardiovascular disease is the leading cause of death worldwide and coronary artery disease is its most prevalent manifestation, associated with high mortality and morbidity. In clinical practice cardiac troponins (cTn) are the cornerstone of the diagnosis, risk stratification and thus selection of the optimal treatment strategy in patients with acute coronary syndrome. According to the third update of the universal definition of myocardial infarction (MI) cTn is the preferred cardiac biomarker of myocardial necrosis in the setting of acute myocardial ischemia. Over the last years newer high sensitivity cardiac troponin (hs-cTn) assays have been developed that are more sensitive than conventional assays, have low limit of detection, low imprecision and low reference limits, but due to variability, the deployment of a standardization and harmonization method is required before their wide use in clinical practice. Recent studies have shown that their utilization seems to improve the diagnostic accuracy detecting MI in patients presenting with chest pain. However, the improved sensitivity comes along with a decreased specificity, though serial cTn measurements and the detection of early changes could improve the specificity and the overall diagnostic performance. Moreover, apart from their use in the diagnosis and risk stratification of MI and acute coronary syndromes, hs-cTn assays seem to have a key role in risk stratification and short and long-term prognosis in a variety of cardiovascular modalities such as stable coronary disease, heart failure and acute pulmonary embolism. In addition, studies have suggested that cTns may be used as a biomarker in the primary prevention of cardiovascular disease leading to the identification of high-risk populations or individuals with silent heart disease.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.