Among the numerous molecules that are being studied for their potential utility as biomarkers of cardiovascular diseases, much interest has been shown in the superfamily of tumor necrosis factor (TNF) receptors. Members of this family include osteoprotegerin (OPG) and its ligands, which are receptor activators of nuclear factor κB ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). These signals may be expressed and regulated, and their functions could be involved in several physiological and pathological processes. The relationship between bone regulatory proteins and vascular biology has attracted attention, and it has been suggested that OPG may mediate vascular calcification and cardiometabolic diseases. OPG is steadily released from vascular endothelial cells in response to inflammatory stimuli, suggesting that it plays a modulatory role in vascular injury, inflammation, and atherosclerosis. Vascular calcification, a hallmark of atherosclerosis, is similar to bone remodeling. It is an actively regulated mechanism that includes both inductive and inhibitory processes. There is a temporal link between the development of osteoporosis and vascular calcification, which is particularly marked in post-menopausal women and the elderly. The precise nature of the link between bone metabolism, vascular calcification and cardiovascular disease is largely unknown but increasing evidence suggests that the triad of RANK/RANKL/OPG may be important in the initiation of various diseases. An increased release of OPG is associated with increased cardiovascular risk and it is suggested that increased OPG levels resulting from vascular damage correspond to a protective mechanism. Circulating OPG levels could be used as independent biomarkers of cardiovascular disease in patients with acute or chronic cardiometabolic disease and thus an improved prognosis.

在被研究作为心血管疾病生物标记物的潜在用途的众多分子中，对肿瘤坏死因子（TNF）受体的超家族表现出了极大的兴趣。该家族的成员包括骨保护素（OPG）及其配体，它们是核因子κB配体（RANKL）和TNF相关凋亡诱导配体（TRAIL）的受体激活剂。这些信号可以被表达和调节，并且它们的功能可能涉及几个生理和病理过程。骨调节蛋白与血管生物学之间的关系已引起人们的关注，并且有人提出OPG可能介导血管钙化和心脏代谢疾病。响应炎症刺激，OPG从血管内皮细胞稳定释放，提示它在血管损伤，炎症和动脉粥样硬化中起调节作用。血管钙化是动脉粥样硬化的标志，与骨骼重塑相似。它是一种主动调节的机制，包括诱导过程和抑制过程。骨质疏松症的发展与血管钙化之间存在时间联系，这在绝经后妇女和老年人中尤为明显。骨代谢，血管钙化和心血管疾病之间联系的确切性质在很大程度上尚不清楚，但越来越多的证据表明，RANK / RANKL / OPG三联征可能在引发各种疾病中起重要作用。OPG释放增加与心血管风险增加有关，提示血管损伤导致OPG水平升高与保护机制相对应。循环OPG水平可用作急性或慢性心脏代谢性疾病患者心血管疾病的独立生物标志物，因此可改善预后。