首先声明一下，我不是医生。甚至基础性科学方面生物生理知识都有限，不过是喜欢可以读一些科学文章。所以想和大家探讨求证一下这个武汉肺炎的病理。
昨晚补了一下ACE2的作用。得出这样的理解：
- Ace 和ace2是腎素-血管收縮素系統里互相制衡的。实验证明ACE2在肺纤毛表面细胞上有很高的表达。在肺里，它帮助调节循环系统里面肾素和血管收缩的素的平衡。（有文献依据）
- 以下是我个人的理解，
- 如果一个人的心肺功能差，体内氧气不足，ACE2在肺部就会过分表达显露出来，这样冠状病毒和Ace2的接触概率就增加了。
- 我认为，如果病毒复制干扰到ACE2正常的功能，会进一步妨碍肺部的氧气吸收能力。
- 如果人体免疫系统去消灭这些被病毒感染的细胞，实际上把ACE 2也消灭了。这些ACE2表达出来的细胞实际上为了人体要提高肺部的吸收能力，致使Ace增加，为了辅助ACE保护肺部细胞不纤化，Ace2也同时增加了。本来Ace2是保护肺细胞的，但是反而被免疫系统一起消灭了。所以病毒对本来心肺功能差，体内氧气含量低的人，伤害更大。是双重打击。
- 那么，作为健康的人，我们是不是应该多到空旷的室外，呼吸新鲜的空气，心情平静地避免给自己的心肺功能造成不必要的stress.
这到应了:正气不足，邪气当道。正气内存，邪不可干。
以下是学术文章的摘要：
ACE2 is more abundantly expressed on the apical surface of polarized epithelia, and we show for the first time that well-differentiated cells support viral replication with viral entry and egress occurring primarily from the apical surface. Thus, SARS-CoV preferentially infects well-differentiated ciliated epithelial cells expressing ACE2. Since ACE2 is also the receptor for the coronavirus NL63 (12), these findings are relevant to the biology of infection with this more common human pathogen.
ACE2 Receptor Expression and Severe Acute Respiratory Syndrome Coronavirus Infection Depend on Differentiation of Human Airway Epithelia
Hong Peng Jia, Dwight C. Look, [...], and Paul B. McCray, Jr
RAS activity is intrinsically high in the lung, which is a major source of ACE and therefore a major site of systemic Ang II synthesis. ACE2 is also highly expressed in the lung. Pulmonary ACE2 appears to have a role in regulating the balance of circulating Ang II/Ang 1–7 levels. (ACE2在肺部有很高的表达。在肺里，它帮助调节循环系统里面肾素和血管收缩的素的平衡）Ang II induces pulmonary vasoconstriction in response to hypoxia, which is important in preventing shunting in patients with pneumonia or lung injury [59]. Locally increased Ang II production also triggers increasing vascular permeability facilitating pulmonary edema [60]. In Acute respiratory distress syndrome (ARDS), the RAS appears crucial in maintaining oxygenation, possibly as widespread lung injury would otherwise result in complete pulmonary shutdown. Certainly in ARDS models, ACE2 knockout mice displayed more severe symptoms of this disease compared with wild-type mice [60] while overexpression appears protective (see below). Interestingly, ACE2 protein also appears to be the entry-point receptor for the severe acute respiratory syndrome (SARS) coronavirus [61, 62].
Review Article | Open Access
Volume 2012 |Article ID 256294 | 8 pages | https://doi.org/10.1155/2012/256294
