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ACE2 下调可能是一种短暂的分子疾病,导致 COVID-19 患者的微循环环境中 RAAS 失调和组织损伤。

ACE2 Down-Regulation May Act as a Transient Molecular Disease Causing RAAS Dysregulation and Tissue Damage in the Microcirculatory Environment Among COVID-19 Patients.

机构信息

Department of Pathology and Forensic Medicine, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.

Department of Pathology and Forensic Medicine, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.

出版信息

Am J Pathol. 2021 Jul;191(7):1154-1164. doi: 10.1016/j.ajpath.2021.04.010. Epub 2021 May 6.

Abstract

Severe acute respiratory syndrome coronavirus 2, the etiologic agent of coronavirus disease 2019 (COVID-19) and the cause of the current pandemic, produces multiform manifestations throughout the body, causing indiscriminate damage to multiple organ systems, particularly the lungs, heart, brain, kidney, and vasculature. The aim of this review is to provide a new assessment of the data already available for COVID-19, exploring it as a transient molecular disease that causes negative regulation of angiotensin-converting enzyme 2, and consequently, deregulates the renin-angiotensin-aldosterone system, promoting important changes in the microcirculatory environment. Another goal of the article is to show how these microcirculatory changes may be responsible for the wide variety of injury mechanisms observed in different organs in this disease. The new concept of COVID-19 provides a unifying pathophysiological picture of this infection and offers fresh insights for a rational treatment strategy to combat this ongoing pandemic.

摘要

严重急性呼吸综合征冠状病毒 2 是 2019 年冠状病毒病(COVID-19)的病原体,也是当前大流行的原因,它在全身产生多种表现,对多个器官系统造成无差别损害,特别是肺、心脏、大脑、肾脏和脉管系统。本综述的目的是提供对 COVID-19 现有数据的新评估,将其视为一种短暂的分子疾病,导致血管紧张素转换酶 2 的负调控,进而使肾素-血管紧张素-醛固酮系统失稳,促进微循环环境的重要变化。本文的另一个目的是展示这些微循环变化如何可能导致这种疾病在不同器官中观察到的广泛损伤机制。COVID-19 的新概念为这种感染提供了统一的病理生理学图像,并为对抗这一持续大流行的合理治疗策略提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/46f8/8099789/f1478ac49e37/gr1_lrg.jpg

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