Abstract
SARS-CoV-2 represents the greatest epidemiological, clinical, and social challenge the human being has had to face in this century. SARS-CoV-2 is not merely a respiratory virus, as its target cells range from upper airway respiratory cells to pulmonary cells but also and above all to the cardiovascular cells, such as pericytes and endothelial cells. Indeed, the pathology related to SARS-CoV-2, COVID-19, may be defined as a thromboinflammatory syndrome in its most severe form, characterized by sepsis-induced coagulopathy (SIC) and disseminated intravascular coagulopathy (DIC), which is prevalent in individuals already presenting a chronic level of inflammation (e.g., obese individuals, elderly) and hypertension. Pregnancy is not only an inflammatory-prone condition but is characterized by a consistent rearrangement of the blood circulation and coagulation profile. Cardiac output increases while arterial systolic and diastolic pressure decrease, regardless of the activation of the RAS system. ACE2, the SARS-CoV-2 entry receptor into the host cells, which transforms Ang II in Ang 1–7, is highly expressed in endothelial, smooth muscle cells and pericytes of placental villi, regulating blood pressure and fetal development. Pre-eclampsia is a pregnancy disorder characterized by hypertension and low levels of ACE2, endothelial dysfunction, and a high production of pro-inflammatory cytokines, resembling COVID-19 manifestations. Whereas pre-eclampsia and COVID-19 have overlapping clinical features, a role for SARS-CoV-2 as a leading cause of pre-eclampsia in COVID-19 positive pregnant women has not been clarified yet. In this mini-review, we will explore the possibility of the existence of such a link, focusing on the role of endothelial dysfunction and RAS in both pre-eclampsia and SARS-CoV-2-induced COVID-19 pathogenesis.
Highlights
Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2), the viral agent causing Coronavirus disease-19 (COVID-19), is a RNA-enveloped β-coronavirus with a high degree of similarity–from 95 to 96%–at the level of the genomic sequence with the bat coronavirus RaTG13 [1]
renin-angiotensin system (RAS) dysregulation, endothelial damage, and hyperinflammation seem to represent common biological phenomena characterizing both COVID-19 and PE. In this mini-review, we focus on the cardiovascular mechanisms malfunctioning in both COVID-19 and PE, possibly underpinning a role of SARS-CoV-2 in the pathogenesis of PE and pre-term-birth in COVID-19 pregnant women, based on the current— poor—available data
It has to be considered that, despite the lack of an outstanding demonstration of SARS-CoV-2 entry into placental cells through Angiotensin Converting Enzyme 2 (ACE2) and TMPRSS2, SARS-CoV2-related systemic inflammation may contribute to the development of pre-eclamptic conditions
Summary
Severe Acute Respiratory Syndrome-Coronavirus-2 (SARS-CoV-2), the viral agent causing Coronavirus disease-19 (COVID-19), is a RNA-enveloped β-coronavirus with a high degree of similarity–from 95 to 96%–at the level of the genomic sequence with the bat coronavirus RaTG13 [1]. Hyperinflammation, which characterizes COVID-19 in its severe form, may locally activate the complement cascade, which, in turn, may directly damage the alveolar endothelium and recruit leukocytes which amplify the inflammatory response [4]. These local phenomena are believed to expand broadly to other organs in the body, like kidneys and brain. RAS dysregulation, endothelial damage, and hyperinflammation seem to represent common biological phenomena characterizing both COVID-19 and PE In this mini-review, we focus on the cardiovascular mechanisms malfunctioning in both COVID-19 and PE, possibly underpinning a role of SARS-CoV-2 in the pathogenesis of PE and pre-term-birth in COVID-19 pregnant women, based on the current— poor—available data
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