SARS-CoV-2 receptor ACE2-dependent implications on the cardiovascular system: From basic science to clinical implications.,Journal of Molecular and Cellular Cardiology

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SARS-CoV-2 receptor ACE2-dependent implications on the cardiovascular system: From basic science to clinical implications.
Journal of Molecular and Cellular Cardiology ( IF 4.9 ) Pub Date : 2020-04-30 , DOI: 10.1016/j.yjmcc.2020.04.031
Sonja Groß ₁ , Christopher Jahn ₁ , Sarah Cushman ₁ , Christian Bär ₂ , Thomas Thum ₂

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The current COVID-19 pandemic started several months ago and is still exponentially growing in most parts of the world - this is the most recent and alarming update. COVID-19 requires the collaboration of nearly 200 countries to curb the spread of SARS-CoV-2 while gaining time to explore and improve treatment options especially for cardiovascular disease (CVD) and immunocompromised patients, who appear to be at high-risk to die from cardiopulmonary failure. Currently unanswered questions are why elderly people, particularly those with pre-existing comorbidities seem to exhibit higher mortality rates after SARS-CoV-2 infection and whether intensive care becomes indispensable for these patients to prevent multi-organ failure and sudden death. To face these challenges, we here summarize the molecular insights into viral infection mechanisms and implications for cardiovascular disease. Since the infection starts in the upper respiratory system, first flu-like symptoms develop that spread throughout the body. The wide range of affected organs is presumably based on the common expression of the major SARS-CoV-2 entry-receptor angiotensin-converting enzyme 2 (ACE2). Physiologically, ACE2 degrades angiotensin II, the master regulator of the renin-angiotensin-aldosterone system (RAAS), thereby converting it into vasodilatory molecules, which have well-documented cardio-protective effects. Thus, RAAS inhibitors, which may increase the expression levels of ACE2, are commonly used for the treatment of hypertension and CVD. This, and the fact that SARS-CoV-2 hijacks ACE2 for cell-entry, have spurred controversial discussions on the role of ACE2 in COVID-19 patients. In this review, we highlight the state-of-the-art knowledge on SARS-CoV-2-dependent mechanisms and the potential interaction with ACE2 expression and cell surface localization. We aim to provide a list of potential treatment options and a better understanding of why CVD is a high risk factor for COVID-19 susceptibility and further discuss the acute as well as long-term cardiac consequences.

中文翻译：

SARS-CoV-2 受体 ACE2 依赖性对心血管系统的影响：从基础科学到临床影响。

当前的 COVID-19 大流行始于几个月前，并且在世界大部分地区仍在呈指数级增长 - 这是最新且令人震惊的更新。COVID-19 需要近 200 个国家的合作来遏制 SARS-CoV-2 的传播，同时争取时间探索和改进治疗方案，特别是针对心血管疾病 (CVD) 和免疫功能低下患者的治疗方案，这些患者似乎面临着高死亡风险来自心肺衰竭。目前尚未解答的问题是，为什么老年人，特别是那些已有合并症的老年人在感染 SARS-CoV-2 后似乎表现出更高的死亡率，以及重症监护是否成为这些患者预防多器官衰竭和猝死所不可或缺的。为了应对这些挑战，我们在此总结了对病毒感染机制及其对心血管疾病影响的分子见解。由于感染始于上呼吸系统，因此首先会出现类似流感的症状，并蔓延至全身。受影响的器官范围广泛可能是由于主要 SARS-CoV-2 进入受体血管紧张素转换酶 2 (ACE2) 的共同表达。从生理学角度来看，ACE2 会降解血管紧张素 II（肾素-血管紧张素-醛固酮系统 (RAAS) 的主要调节剂），从而将其转化为血管舒张分子，这种分子具有已被充分证明的心脏保护作用。因此，RAAS抑制剂可能会增加ACE2的表达水平，通常用于治疗高血压和CVD。这一事实，以及 SARS-CoV-2 劫持 ACE2 进入细胞的事实，引发了关于 ACE2 在 COVID-19 患者中的作用的争议性讨论。在这篇综述中，我们重点介绍了有关 SARS-CoV-2 依赖性机制以及与 ACE2 表达和细胞表面定位的潜在相互作用的最新知识。我们的目标是提供一系列潜在的治疗方案，更好地理解为什么 CVD 是 COVID-19 易感性的高危因素，并进一步讨论急性和长期的心脏后果。

更新日期：2020-04-30

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