Abstract
The course of the COVID-19 pandemic has led to high mortality rates worldwide, which justifies the development of various research studies aimed at elucidating the physiopathological mechanisms involved in the development of lung injury associated with this disease. The angiotensin-converting enzyme 2 (ACE2) receptor plays a leading role as the viral anchoring point necessary for viral replication to begin, so a thorough understanding of the regulatory mechanisms of this receptor is vital. Similarly, the distribution of ACE2 will justify the injury caused by SARS-CoV-2. Macrophages play a more significant role in lung injury since they allow the SARS-CoV-2 virus to reach tissues lacking ACE2 receptors and cause significant tissue damage. Therefore, all factors that influence macrophage migration and mobilization will be considered risk factors for the development of severe lung injury in COVID-19.
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