Heart failure (HF) is considered one of the most common diseases and one of the major causes of death. The latest studies show that HF is associated with an increase in oxidative stress. The use of antioxidants as therapy is effective in animal models, but not in humans. In this review, we analyse some emerging markers related to oxidative stress, evaluating their possible use as therapeutic targets: galectin-3, a β galactoside associated with myocardial fibrosis, α1-antitrypsin, an antiprotease and lectin-like oxidized low-density-lipoprotein receptor-1, the major receptor for ox-LDL. The up-regulation of galectin-3 appears to be associated with HF, atrial fibrillation, dilated cardiomyopathy, fibrogenesis and mortality, while in other cases it seems that galectin-3 may be protective in ischaemia-reperfusion injury. Serum α1-antitrypsin protein levels may increase in the presence of high concentrations of serum proteases, which are over expressed during reperfusion. The overexpression of α1-antitrypsin or the exogenous α1-antitrypsin treatment exhibits an anti-oxidative stress role, evaluated by increased eNOS expression and by decreased MMP9 expression, implicated in HF. The cardiac lectin-like oxidized low-density-lipoprotein receptor-1 is activated by oxidative stress in ischaemia-reperfusion injury, inducing apoptosis in cardiomyocytes through the deleterious NF-kB pathway, while the administration of anti-lectin-like oxidized low-density-lipoprotein receptor-1 antibody suppresses apoptosis and reduces the extent of myocardial infarction. In conclusion, α1-antitrypsin and lectin-like oxidized low-density-lipoprotein receptor-1 seem to represent two good markers in HF and therapeutic targets, whereas galectin-3 does not.

中文翻译：

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氧化应激相关生物标志物在心力衰竭中的作用：半乳凝素3，α1-抗胰蛋白酶和LOX-1：新的治疗方法？

心力衰竭（HF）被认为是最常见的疾病之一，也是主要的死亡原因之一。最新研究表明，HF与氧化应激的增加有关。使用抗氧化剂作为治疗剂在动物模型中有效，但在人类中却无效。在这篇综述中，我们分析了一些与氧化应激有关的新兴标志物，评估了它们可能作为治疗靶点的用途：galectin-3，与心肌纤维化相关的β-半乳糖苷，α1-抗胰蛋白酶，抗蛋白酶和凝集素样氧化的低密度脂蛋白受体1，ox-LDL的主要受体。galectin-3的上调似乎与心衰，心房纤颤，扩张型心肌病，纤维化和死亡率有关，而在其他情况下，galectin-3可能在缺血再灌注损伤中起保护作用。在高浓度血清蛋白酶的存在下，血清α1-抗胰蛋白酶的蛋白水平可能会升高，而在再灌注过程中它们会过度表达。α1-抗胰蛋白酶的过表达或外源性α1-抗胰蛋白酶的处理均表现出抗氧化应激作用，可通过与HF相关的eNOS表达增加和MMP9表达减少来评估。缺血-再灌注损伤中的氧化应激激活心脏凝集素样氧化型低密度脂蛋白受体-1，并通过有害的NF-kB途径诱导心肌细胞凋亡，而施用抗凝集素样氧化型低密度蛋白-脂蛋白受体1抗体抑制细胞凋亡并减少心肌梗塞的程度。结论，