PDF(Pubmed)
Abstract：
Severe Acute Respiratory Syndrome Corona Virus 2 (SARS-CoV-2) infecting mechanism depends on hosting angiotensin-converting enzyme 2 (ACE2) and transmembrane protease serine 2 (TMPRSS2) as essential components and androgens as regulators for inducing the expression of these components. Therefore, hyperandrogenism-related disease such as polycystic ovary syndrome (PCOS) in insulin resistant women in reproductive-age is a high-risk factor for SARS-CoV-2 infection. Here, we describe the signaling pathways that might increase the susceptibility and severity of this new pandemic in PCOS women with insulin resistance (IR). Luteinizing hormone and insulin increase the risk of SARS-CoV-2 infection in these patients via the induction of steroidogenic enzymes expression through cAMP-response element binding protein and Forkhead box protein O1 (FOXO1), respectively. TMPRSS2 expression is activated through phosphorylation of FOXO1 in ovaries. In other words, SARS-CoV-2 infection is associated with temporary IR by affecting ACE2 and disturbing β-pancreatic function. Therefore, PCOS, IR, and SARS-CoV-2 infection are three corners of the triangle that have complicated relations, and their association might increase the risk of SARS-CoV-2 infection and severity.
摘要：
严重急性呼吸综合征冠状病毒2（SARS-CoV-2）的感染机制取决于将血管紧张素转换酶2（ACE2）和跨膜蛋白酶丝氨酸2（TMPRSS2）作为必需成分，并将雄激素作为诱导表达的调节剂。这些成分。因此,育龄期胰岛素抵抗妇女的高雄激素血症相关疾病如多囊卵巢综合征(PCOS)是SARS-CoV-2感染的高危因素.这里,我们描述了在有胰岛素抵抗(IR)的PCOS女性中,可能增加这种新的流行病的易感性和严重性的信号通路.黄体生成素和胰岛素通过cAMP反应元件结合蛋白和叉头盒蛋白O1（FOXO1）诱导类固醇生成酶的表达，增加了这些患者SARS-CoV-2感染的风险，分别。TMPRSS2表达通过卵巢中FOXO1的磷酸化而被激活。换句话说,SARS-CoV-2感染通过影响ACE2和干扰β-胰腺功能而与暂时性IR相关。因此,PCOS,IR,和SARS-CoV-2感染是三角形的三个角落，有着复杂的关系，它们的关联可能会增加SARS-CoV-2感染的风险和严重程度。
