Arauna Diego, Navarrete Simón, Albala Cecilia, Wehinger Sergio, Pizarro-Mena Rafael, Palomo Iván, Fuentes Eduardo
Thrombosis Research and Healthy Aging Center, Department of Clinical Biochemistry and Immunohematology, Interuniversity Center for Healthy Aging (CIES), Interuniversity Network of Healthy Aging in Latin America and Caribbean (RIES-LAC), Faculty of Health Sciences, Universidad de Talca, Talca 3460000, Chile.
Unidad de Nutrición Pública, Instituto de Nutrición y Tecnología de los Alimentos, Interuniversity Center for Healthy Aging, Universidad de Chile, Santiago 7810000, Chile.
Biomedicines. 2024 Sep 3;12(9):2004. doi: 10.3390/biomedicines12092004.
Frailty and cardiovascular diseases are increasingly prevalent in aging populations, sharing common pathological mechanisms, such as oxidative stress. The evidence shows that these factors predispose frail individuals to cardiovascular diseases but also increase the risk of thrombosis. Considering this background, this review aims to explore advances regarding the relationship between oxidative stress, platelet alterations, and cardiovascular diseases in frailty, examining the role of reactive oxygen species overproduction in platelet activation and thrombosis. The current evidence shows a bidirectional relationship between frailty and cardiovascular diseases, emphasizing how frailty not only predisposes individuals to cardiovascular diseases but also accelerates disease progression through oxidative damage and increased platelet function. Thus, oxidative stress is the central axis in the increase in platelet activation and secretion and the inadequate response to acetylsalicylic acid observed in frail people by mitochondrial mechanisms. Also, key biomarkers of oxidative stress, such as isoprostanes and derivate reactive oxygen metabolites, can be optimal predictors of cardiovascular risk and potential targets for therapeutic intervention. The potential of antioxidant therapies in mitigating oxidative stress and improving cardiovascular clinical outcomes such as platelet function is promising in frailty, although further research is necessary to establish the efficacy of these therapies. Understanding these mechanisms could prove essential in improving the health and quality of life of an aging population faced with the dual burden of frailty and cardiovascular diseases.
衰弱和心血管疾病在老年人群中日益普遍，它们有着共同的病理机制，如氧化应激。证据表明，这些因素使衰弱个体易患心血管疾病，同时也增加了血栓形成的风险。考虑到这一背景，本综述旨在探讨衰弱状态下氧化应激、血小板改变与心血管疾病之间关系的研究进展，研究活性氧过度产生在血小板活化和血栓形成中的作用。目前的证据表明衰弱与心血管疾病之间存在双向关系，强调了衰弱不仅使个体易患心血管疾病，还通过氧化损伤和血小板功能增强加速疾病进展。因此，氧化应激是导致衰弱人群血小板活化和分泌增加以及对乙酰水杨酸反应不足的核心因素，其机制与线粒体有关。此外，氧化应激的关键生物标志物，如异前列腺素和衍生的活性氧代谢产物，可能是心血管风险的最佳预测指标和治疗干预的潜在靶点。抗氧化疗法在减轻氧化应激和改善心血管临床结局（如血小板功能）方面的潜力在衰弱人群中很有前景，不过还需要进一步研究来确定这些疗法的疗效。了解这些机制对于改善面临衰弱和心血管疾病双重负担的老年人群的健康和生活质量可能至关重要。
