Department of Medical Sciences, School of Medicine at Ciudad Real, University of Castilla-La Mancha, 13971 Ciudad Real, Spain.
Facultad HM de Ciencias de la Salud, Universidad Camilo José Cela, 28692 Madrid, Spain.
Int J Mol Sci. 2024 Jul 10;25(14):7553. doi: 10.3390/ijms25147553.
Proteases are produced and released in the mucosal cells of the respiratory tract and have important physiological functions, for example, maintaining airway humidification to allow proper gas exchange. The infectious mechanism of severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), which causes coronavirus disease 2019 (COVID-19), takes advantage of host proteases in two ways: to change the spatial conformation of the spike (S) protein via endoproteolysis (e.g., transmembrane serine protease type 2 (TMPRSS2)) and as a target to anchor to epithelial cells (e.g., angiotensin-converting enzyme 2 (ACE2)). This infectious process leads to an imbalance in the mucosa between the release and action of proteases versus regulation by anti-proteases, which contributes to the exacerbation of the inflammatory and prothrombotic response in COVID-19. In this article, we describe the most important proteases that are affected in COVID-19, and how their overactivation affects the three main physiological systems in which they participate: the complement system and the kinin-kallikrein system (KKS), which both form part of the contact system of innate immunity, and the renin-angiotensin-aldosterone system (RAAS). We aim to elucidate the pathophysiological bases of COVID-19 in the context of the imbalance between the action of proteases and anti-proteases to understand the mechanism of aprotinin action (a panprotease inhibitor). In a second-part review, titled "Aprotinin (II): Inhalational Administration for the Treatment of COVID-19 and Other Viral Conditions", we explain in depth the pharmacodynamics, pharmacokinetics, toxicity, and use of aprotinin as an antiviral drug.
蛋白酶在呼吸道黏膜细胞中产生并释放,具有重要的生理功能,例如维持气道湿润以实现适当的气体交换。导致 2019 冠状病毒病(COVID-19)的 2 型严重急性呼吸综合征冠状病毒(SARS-CoV-2)的感染机制利用宿主蛋白酶有两种方式:通过内肽酶(例如跨膜丝氨酸蛋白酶 2(TMPRSS2))改变刺突(S)蛋白的空间构象,以及作为锚定到上皮细胞的靶点(例如血管紧张素转换酶 2(ACE2))。这个感染过程导致黏膜中蛋白酶的释放和作用与抗蛋白酶的调节之间失去平衡,这导致 COVID-19 中炎症和促血栓形成反应加剧。在本文中,我们描述了在 COVID-19 中受影响的最重要的蛋白酶,以及它们的过度激活如何影响它们参与的三个主要生理系统:补体系统和激肽-血管舒缓素系统(KKS),它们都构成固有免疫接触系统的一部分,以及肾素-血管紧张素-醛固酮系统(RAAS)。我们旨在阐明 COVID-19 中蛋白酶和抗蛋白酶作用失衡的病理生理基础,以了解抑肽酶(一种广谱蛋白酶抑制剂)的作用机制。在题为“抑肽酶(II):用于治疗 COVID-19 和其他病毒病的吸入给药”的第二部分综述中,我们深入解释了抑肽酶作为抗病毒药物的药效学、药代动力学、毒性和用途。