Shukla Ashwin Kumar, Awasthi Komal, Usman Kauser, Banerjee Monisha
Molecular and Human Genetics Laboratory, Department of Zoology, University of Lucknow, Lucknow 226007, Uttar Pradesh, India.
Department of Medicine, King Georges' Medical University, Lucknow 226003, Uttar Pradesh, India.
World J Diabetes. 2024 Apr 15;15(4):606-622. doi: 10.4239/wjd.v15.i4.606.
Coronavirus disease 2019 (COVID-19) is a disease that caused a global pandemic and is caused by infection of severe acute respiratory syndrome coronavirus 2 virus. It has affected over 768 million people worldwide, resulting in approximately 6900000 deaths. High-risk groups, identified by the Centers for Disease Control and Prevention, include individuals with conditions like type 2 diabetes mellitus (T2DM), obesity, chronic lung disease, serious heart conditions, and chronic kidney disease. Research indicates that those with T2DM face a heightened susceptibility to COVID-19 and increased mortality compared to non-diabetic individuals. Examining the renin-angiotensin system (RAS), a vital regulator of blood pressure and pulmonary stability, reveals the significance of the angiotensin-converting enzyme (ACE) and ACE2 enzymes. ACE converts angiotensin-I to the vasoconstrictor angiotensin-II, while ACE2 counters this by converting angiotensin-II to angiotensin 1-7, a vasodilator. Reduced ACE2 expression, common in diabetes, intensifies RAS activity, contributing to conditions like inflammation and fibrosis. Although ACE inhibitors and angiotensin receptor blockers can be therapeutically beneficial by increasing ACE2 levels, concerns arise regarding the potential elevation of ACE2 receptors on cell membranes, potentially facilitating COVID-19 entry. This review explored the role of the RAS/ACE2 mechanism in amplifying severe acute respiratory syndrome coronavirus 2 infection and associated complications in T2DM. Potential treatment strategies, including recombinant human ACE2 therapy, broad-spectrum antiviral drugs, and epigenetic signature detection, are discussed as promising avenues in the battle against this pandemic.
2019冠状病毒病(COVID-19)是一种引发全球大流行的疾病,由严重急性呼吸综合征冠状病毒2病毒感染所致。它已影响全球超过7.68亿人,导致约690万人死亡。美国疾病控制与预防中心确定的高危人群包括患有2型糖尿病(T2DM)、肥胖症、慢性肺病、严重心脏病和慢性肾病等疾病的个体。研究表明,与非糖尿病个体相比,T2DM患者对COVID-19的易感性更高,死亡率也更高。研究肾素-血管紧张素系统(RAS)——血压和肺稳定性的重要调节因子,揭示了血管紧张素转换酶(ACE)和ACE2酶的重要性。ACE将血管紧张素-I转化为血管收缩剂血管紧张素-II,而ACE2则通过将血管紧张素-II转化为血管扩张剂血管紧张素1-7来对抗这一过程。糖尿病患者中常见的ACE2表达降低会增强RAS活性,导致炎症和纤维化等病症。尽管ACE抑制剂和血管紧张素受体阻滞剂可通过提高ACE2水平带来治疗益处,但人们担心细胞膜上ACE2受体可能会增加,从而可能促进COVID-19进入细胞。本综述探讨了RAS/ACE2机制在加剧严重急性呼吸综合征冠状病毒2感染及T2DM相关并发症中的作用。文中讨论了包括重组人ACE2疗法、广谱抗病毒药物和表观遗传特征检测在内的潜在治疗策略,认为这些是对抗这一全球大流行的有前景的途径。