Membrane endoglin (Eng, CD105) is a transmembrane glycoprotein essential for the proper function of vascular endothelium. It might be cleaved by matrix metalloproteinases to form soluble endoglin (sEng), which is released into the circulation. Metabolic syndrome comprises conditions/symptoms that usually coincide (endothelial dysfunction, arterial hypertension, hyperglycemia, obesity-related insulin resistance, and hypercholesterolemia), and are considered risk factors for cardiometabolic disorders such as atherosclerosis, type II diabetes mellitus, and liver disorders. The purpose of this review is to highlight current knowledge about the role of Eng and sEng in the disorders mentioned above, in vivo and in vitro extent, where we can find a wide range of contradictory results. We propose that reduced Eng expression is a hallmark of endothelial dysfunction development in chronic pathologies related to metabolic syndrome. Eng expression is also essential for leukocyte transmigration and acute inflammation, suggesting that Eng is crucial for the regulation of endothelial function during the acute phase of vascular defense reaction to harmful conditions. sEng was shown to be a circulating biomarker of preeclampsia, and we propose that it might be a biomarker of metabolic syndrome-related symptoms and pathologies, including hypercholesterolemia, hyperglycemia, arterial hypertension, and diabetes mellitus as well, despite the fact that some contradictory findings have been reported. Besides, sEng can participate in the development of endothelial dysfunction and promote the development of arterial hypertension, suggesting that high levels of sEng promote metabolic syndrome symptoms and complications. Therefore, we suggest that the treatment of metabolic syndrome should take into account the importance of Eng in the endothelial function and levels of sEng as a biomarker and risk factor of related pathologies.

膜内皮因子（Eng，CD105）是一种跨膜糖蛋白，对于血管内皮的正常功能至关重要。它可能被基质金属蛋白酶裂解形成可溶性内皮糖蛋白 (sEng)，并释放到循环中。代谢综合征包括通常同时出现的病症/症状（内皮功能障碍、动脉高血压、高血糖、肥胖相关的胰岛素抵抗和高胆固醇血症），并且被认为是心脏代谢疾病（例如动脉粥样硬化、II型糖尿病和肝脏疾病）的危险因素。本综述的目的是强调当前关于 Eng 和 sEng 在上述疾病中的作用的知识，在体内和体外范围内，我们可以发现各种相互矛盾的结果。我们认为，Eng 表达减少是代谢综合征相关慢性病理中内皮功能障碍发展的标志。 Eng 表达对于白细胞迁移和急性炎症也至关重要，这表明 Eng 对于血管对有害条件的防御反应的急性期内皮功能的调节至关重要。 sEng 被证明是先兆子痫的循环生物标志物，我们认为它可能是代谢综合征相关症状和病理的生物标志物，包括高胆固醇血症、高血糖、动脉高血压和糖尿病，尽管事实上存在一些相互矛盾的发现已被报道。此外，sEng可以参与内皮功能障碍的发生并促进动脉高血压的发生，表明高水平的sEng可促进代谢综合征症状和并发症。 因此，我们建议代谢综合征的治疗应考虑Eng在内皮功能中的重要性以及sEng水平作为相关病理的生物标志物和危险因素。