Rev Invest Clin
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Obstructive sleep apnea is characterized by total or partial interruptions of airflow during sleep, despite ongoing efforts to breathe. These pauses result from repeated upper airway obstructions that generate a systemic inflammatory condition with consequences for the endothelial function that increase the risk of cardiometabolic events. The prevalence of obstructive sleep apnea during pregnancy is greater than that observed in the general population and increases in the third trimester. ⋯ Experimental and prospective studies in humans have demonstrated an association between obstructive sleep apnea and low birth weight. Endothelial dysfunction may be the link that underlies the association of obstructive sleep apnea with high perinatal risk. The information reviewed herein suggests that treating obstructive sleep apnea with positive-pressure devices could be an effective strategy for decreasing perinatal morbidity and mortality.
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Idiopathic pulmonary fibrosis is a chronic, progressive, and usually fatal lung disorder of unknown etiology. The disease likely results from the interaction of genetic susceptibility architecture, environmental factors such as smoking, and an abnormal epigenetic reprogramming that leads to a complex pathogenesis. ⋯ Recently, nine molecular and cellular hallmarks of aging have been proposed: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. In this review, we provide an overview of these molecular mechanisms and their involvement in the pathogenesis of idiopathic pulmonary fibrosis, while emphasizing that the studies on this disease are few and the findings are not definitive.
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Aging is a complex phenomenon leading to numerous changes in the physiological systems of the body. One of the most important changes, called immunosenescence, occurs in the immune system. ⋯ The origin of this inflammaging is not known with certainty, but several concurrent contributing factors have been suggested, such as aging-associated changes in the innate and adaptive immune response, chronic antigenic stimulation, the appearance of endogenous macromolecular changes, and the presence of senescent cells exhibiting a senescence-associated secretory phenotype. A better understanding of the multiple biological phenomena leading to these diseases via the immunosenescence associated with inflammaging provides a powerful target for interventions to increase the healthspan of elderly subjects.
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There are several immunological and non-immunological factors related to renal graft deterioration, and histological lesions such as interstitial fibrosis and tubular atrophy overlap with those observed in aging kidneys. Consequently, it has been proposed that kidney transplant senescence could contribute to graft loss. ⋯ Moreover, renal tissue injury predisposes the older graft not only to progressive deterioration due to glomerular hyperfiltration, but also triggers acute rejection due to increased immunogenicity. In conclusion, renal graft senescence is a complex process, and its better understanding will help the nephrologist in its management in order to achieve a longer graft survival.
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The relationship between frailty and cognitive impairment has been recognized for decades, but it was not until a few years ago that the interest in this relationship increased and is now being understood. Epidemiological evidence suggests that physical frailty may be linked to cognitive impairment since both conditions share pathophysiological mechanisms at the cellular and systemic levels. ⋯ However, full understanding of the mechanisms underlying the relationship between frailty and vascular cognitive impairment remains fragmented. This review examines the link between frailty and vascular cognitive decline and also explores the role of vascular changes in the genesis of both conditions.