Aging causes structural and functional decrements in skeletal muscles (sarcopenia), bone mineral density, cardiovascular and oxygen uptake. Progress of many cardiovascular diseases as atherosclerosis, endothelial dysfunction and hypertension with aging. This points out that aging should be seen as a risk factor. This is causes an imbalance between vasodilator-vasoconstriction substances ratio formed by the endothelium resulting in a significant reduction in nitric oxide production. Nitric oxide decrement causes some anomalies in blood artery function along, with an increase in oxidative stress molecules production, which in turn increase production of ROS and nitrogen species. Secreted klotho regulates nitric oxide production which in turn benefits endothelial function: membrane klotho acts through (FGF)-23, while secreted klotho regulates nitric oxide produced in the endothelium. Exercise inactivity accelerates aging and its consequences, it is suggested as a major reason for increased disease and mortality. In recent years however, there are enough studies about the effect of aerobic exercise on blood circulating s-Klotho. Recently, it has been demonstrated that the response of circulating s-klotho depends on aerobic fitness level: values of s-Klotho were significantly higher in trained individuals compared to untrained once, suggesting that aerobic exercise training is a suitable model for mechanistically probing the role of physical activity on s-Klotho expression. In conclusions, the present review suggests that aerobic exercise delays aging process by increase Klotho gene expression, which in turn, reduces ROS damages to the cell. The relationships between the circulating s-Klotho levels a potential anti-aging factor and aerobic exercise are beneficial to physically active aged individuals. Endothelial dysfunction improvement depends on increased circulating s-klotho levels through aerobic exercise. The purpose of this review is to discuss factors such as, oxidative stress and pro-inflammatory cytokines involved in the progress of endothelial dysfunction due to the aging process, with impacts related to, s-Klotho and aerobic exercise on the endothelial dysfunction process.
Keywords: Nitric oxide; Arteriosclerosis; Hypertension; Apoptosis; Oxidative stress; FGF23
Aging considerations
Aging is a usual life course that includes all physiological systems, seen as an advanced biological degeneration and decrease in physical capacities that raises the possibility of disease. Aging is a gradual decline of various organ functions of the body, deteriorating phenomenon defined by relations between the genetic expressions and external factors [1]. Ecological epigenetics defines how natural factors affect cellular epigenetics and, thus, human performance [2]. Aging is a multifaceted process that not only involves the natural biological processes of aging, but also the increased risk for different diseases such as coronary heart disease, diabetes and cancer [3]. The primary aging course, itself genetically related, occurs both independently of life style and in the absence of disease [4]. Aging causes structural changes and functional decrements in skeletal muscles (sarcopenia), bone mineral density, cardiovascular and oxygen delivery. Age-related declines are manifest by a decreased ability for aged skeletal muscle to respond to physiological loads such as muscle loading or acute injury. Indeed, older adults often exhibit an age-related reduction in the number and size of muscle fibers, known as sarcopenia [5]. Accordingly, at maximal effort decreases in maximal cardiac output, arteriovenous oxygen difference and maximal oxygen uptake are noted [6,7]. These age modifications are the balance between cellular impairment due to metabolic measures happening inside the cell and offsetting molecular responses that can restore the damage. It is widely accepted that aging is an important risk factor for the development of hypertension and atherosclerosis with its vascular complications. The underlying mechanism whereby aging elevates the probability of disease onset remains obscure; however, it is likely closely related to underlying mechanisms of atherogenesis, the most accepted being the oxidation hypothesis [8]. In brief, a vital phase in the progress of atherosclerosis is oxidative alteration of low-density lipoprotein. The oxidation of low-density lipoprotein is a free radical driven lipid peroxidation process and the aldehyde products of lipid hydroperoxide breakdown are responsible for the modification of the low-density lipoprotein apoprotein.Successful aging is a function of both genetic and environmental factors [10]. The primary aging process, which is genetically associated, occurs both independently of life style and in the absence of disease [7]. Aging-related changes occur mainly in the cardiopulmonary and skeletal muscles, bringing about a reduction in physical performance [11]. Maximal work capacity is decreased regardless of lifestyle because of genetic factors. Such consequences contribute to the geriatric syndrome of frailty, thereby severely limiting the function, quality of life and longevity [12].
Muscle mass decreased significantly in aged individuals, after the sixth or seventh decades of life, [13].
This reduction in muscle mass is a major factor in the decline of maximal oxygen uptake, indicating the cardiopulmonary fitness of the individual [14], and therefore, bringing about a reduction in physical work capacity [11]. Such myocardial and peripheral functional changes include a decline in the maximum heart rate, stroke volume, and left ventricular contractility, and an increase in total peripheral resistance. Consequently, oxygen delivery to the working muscle decreases. The human population aged from 0 to 91 years screened previously by ELISA revealed that the level of s-Klotho was related to human physiological declines with aging.
Oxidatively altered low density lipoproteins cause lipidladen macrophage, or foam cell, buildup in the fatty strip, an atherosclerosis process begins. Following employment of immune cells, a pro-inflammatory stage, raises oxidative stress, and starts a sequence of actions including apoptotic vascular and nonvascular cells [16]. It has been suggested that up to 2% of the oxygen utilized (hyperoxide) in the cell’s mitochondria may produce oxygen radicals and peroxisomal level to increase, which may hit and alter DNA, protein, cell membranes and organelles as well as extracellular components [17]. Peroxisomal disorders are inherited diseases representing a group of genetic diseases in humans in which there is a lack of one or more peroxisomal functions [18].
Peroxisomes known as a microbody are organelles containing peroxide enzymes and have distinguishing assignments such as fatty acids breakdown [19]. Peroxisomes are found mainly in the liver and the kidneys, the organs mainly responsible for removing toxic chemicals. Peroxisome carries out oxidation reactions, producing the toxic hydrogen peroxide (H2O2). In addition, peroxisomes hold the enzyme catalase, which causes toxic H2O2 elimination by converting it to H2O and O2 [20]. Peroxisomes as well, is important for energy metabolism and is involved in the enzymatic activity of the pentose (5-carbon sugars) phosphate pathway. It is a metabolic pathway producing nicotinamide adenine dinucleotide phosphate (NADPH) and pentoses as well as ribose 5-phosphate, the last one serves as a precursor for the synthesis of nucleotides.
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