Abstract
Increased oxidative stress from both mitochondrial and cytosolic sources contributes to the development and the progression of cardiovascular diseases (CVDs), and it is a target of therapeutic interventions. The numerous efforts made over the last decades in order to develop tools able to monitor the oxidative stress level in patients affected by CVDs rely on the need to gain information on the disease state. However, this goal has not been satisfactorily accomplished until now. Among others, the isolation of circulating leukocytes to measure their oxidant level offers a valid, noninvasive challenge that has been tested in few pathological contexts, including hypertension, atherosclerosis and its clinical manifestations, and heart failure. Since leukocytes circulate in the blood stream, it is expected that they might reflect quite closely both systemic and cardiovascular oxidative stress and provide useful information on the pathological condition. The results of the studies discussed in the present review article are promising. They highlight the importance of measuring oxidative stress level in circulating mononuclear cells in different CVDs with a consistent correlation between degree of oxidative stress and severity of CVD and of its complications. Importantly, they also point to a double role of leukocytes, both as a marker of disease condition and as a direct contributor to disease progression. Finally, they show that the oxidative stress level of leukocytes reflects the impact of therapeutic interventions. It is likely that the isolation of leukocytes and the measurement of oxidative stress, once adequately developed, may represent an eligible tool for both research and clinical purposes to monitor the role of oxidative stress on the promotion and progression of CVDs, as well as the impact of therapies.
Highlights
Oxidative stress is the product of several intracellular sources such as mitochondrial electron transport chain (ETC), nicotinamide adenine dinucleotide phosphate oxidase (NADPH), nitric oxide synthase, and xanthine oxidase [1,2,3,4]
The combination of extreme dipper and of morning surge blood pressure (BP) types led to an even higher level of reactive oxygen species (ROS) formation. These findings indicate that higher ROS formation from leukocytes in extreme dipper and morning surge BP types is a marker of predisposition to early morning cardiovascular events (CVE)
It has been shown that the use of benidipine reduced oxidative stress in polymorphonuclear leukocyte (PMN) of hypertensive patients, at least in part by reducing BP levels [35], and that angiotensin II type 1 receptor (AT1R) blockers were able to normalize BP and to reduce the oxidative stress produced by leukocytes, suggesting that the latter plays an active role in the pathogenesis of hypertension through the production of oxidative stress
Summary
Oxidative stress is the product of several intracellular sources such as mitochondrial electron transport chain (ETC), nicotinamide adenine dinucleotide phosphate oxidase (NADPH), nitric oxide synthase, and xanthine oxidase [1,2,3,4]. Therapeutic purposes since changes in oxidative stress level parallel the progression of the pathological condition as well as the response to treatment In this regard, a major limitation is obviously represented by the limited availability of tissue samples from both heart and blood vessels so that the use of circulating markers able to represent the condition within the cardiovascular system could overcome the problem. It is likely that this method, once adequately developed, may provide an eligible tool for both research and clinical purposes to examine the role of several oxidative stress-related mechanisms in the promotion and progression of CVDs. The present review article is aimed at discussing the relevance of studies of circulating leukocytes in all major CVDs, from arterial hypertension to ischaemic heart disease and to the final stage of heart failure (Table 1).
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