As the COVID-19 pandemic drags on, scientists worldwide are racing to understand how the virus affects the body. Caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), COVID-19 brings devastating consequences on economic and social fields throughout all continents.
Having better pathophysiological knowledge about the disease is essential for better planning of mitigation measures, diagnosis, and treatment.
Vinicius Novaes Rocha, a researcher at the Federal University of Juiz de Fora in Brazil, provides an insight into the role of the renin-angiotensin on the pathophysiology of COVID-19, paving the way for developing new treatment methods in the journal Medical Hypotheses.
What is the renin-angiotensin-aldosterone?
The renin-angiotensin-aldosterone system (RAAS) is a pivotal hormone system in regulating blood pressure and fluid balance. It comprises of three hormones – renin, angiotensin II, and aldosterone.
RAAS also plays an important role in regulating blood volume and systemic vascular resistance, influencing arterial pressure, and cardiac output. It has been one of the focuses of worldwide research due to the COVID-19 pandemic, which has infected over 40 million people and claimed more than 1.11 million lives since it began in December 2019.
One of the RAAS components, the angiotensin-converting enzyme 2 (ACE2), is widely studied as it has been directly tied to the SARS-CoV-2 infection. ACE2 is the cellular gateway used by the virus to enter and infect human cells. From there, the virus proliferates in the body, which may cause life-threatening complications in some people.
The researcher noted that ACE2 is an important piece in the COVID-19 pathophysiology since the high replication rate of SARS-CoV-2 is directly associated with ACE2 and cell infection coupling. Some studies have shown that the virus also leads to the reduction of ACE2 in the infected organs. Hence, the higher the amount of virus, the higher will be the use of ACE2 by it, creating an inverse correlation between the virus and ACE2.
The RAAS is classified as systemic and local, and the interaction between them is essential to maintaining the body’s balance or homeostasis. The interaction between the local and systemic RAAS may happen via the circulation of soluble ACE and ACE2.
The study author also found that SARS-CoV-2 exhibits a low immune and inflammatory response. He concluded that the more evidence pathogenesis of COVID-19 is related to the RAAS misbalance than the action of the virus itself.
Though this is only a hypothesis, the researcher said there is strong evidence that the fibrotic, inflammatory, and thrombotic processes found in COVID-19 may be related to the inflammatory process caused by the pathogen itself. Hence, the researcher claims that the hypothesis seeks to reaffirm the important role of ACE2 on the pathophysiology of COVID-19.
“A better understanding of COVID-19 pathophysiology is imperative to elaborate on strategies during the pandemic. Thus, this work seeks to enlarge the discussion related to COVID-19, offering alternative ways for experimental and clinical studies aiming at the formulation of new diagnosis or treatment methods,” the author wrote in the paper.
As the pandemic evolves, many countries have reported rising cases of COVID-19. The United States remains the country with the highest number of cases, reaching 8.2 million and at least 220,000 deaths.
The other cases with the highest number of cases include India, with more than 7.55 million cases, Brazil, with more than 5.23 million cases, Russia, with more than 1.40 million.