The Cardiac Effects of COVID-19: Review of articles.

Cardiovascular wellbeing has been dramatically affected by severe acute respiratory syndrome coronavirus (SARS-CoV-2), the reason for the coronavirus disease pandemic 2019 (COVID-19) pandemic. There is a greater risk of morbidity and death in individuals with preexisting heart diseases. Clinical syndromes of the acute coronary syndrome, acute myocardial injury, myocarditis, arrhythmias, heart failure, and venous thromboembolism can, directly and indirectly, affect the heart. There may also be adverse heart effects of specific therapeutics under review for COVID-19. The renin-angiotensin-aldosterone system (RAAS) mechanism in virus replication makes it essential to understand the consequences of the system-modulating medications. For optimum patient care, detailed knowledge of specific cardiovascular symptoms of COVID-19 and the role of RAAS in the prognosis of COVID-19 disease is necessary.

The renin-angiotensin system in cutaneous hypertrophic scar and keloid formation.

Hypertrophic scar and keloid are two types of fibroproliferative conditions that result from excessive extracellular matrix production. The underlying pathological mechanism is not entirely clear. Activation of the renin-angiotensin system (RAS) is associated with fibrosis in various organs. RAS components including angiotensin II (Ang II), angiotensin AT1 and AT2 receptors, and angiotensin-converting enzyme (ACE) are expressed in the skin and act independently from the plasma RAS. AT1 receptors, which are usually the dominating receptor subtype, promote fibrosis and scar formation, while AT2 receptors inhibit the aforementioned AT1 receptor-coupled effects. Elevated angiotensin II (Ang II) levels acting on the AT1 receptor contribute to skin scar formation through increased expression of inflammatory factors such as interleukin-6 (IL-6), angiogenic factors such as vascular endothelial growth factor (VEGF) and fibrinogenic factors such as transforming growth factor-ß1 (TGF-ß1) and connective tissue growth factor (CTGF), while at the same time suppressing the anti-fibrotic tissue inhibitors of matrix metalloproteinase (TIMPs). First, small clinical trials have provided evidence that inhibition of the ACE/Ang II/ AT1 receptor axis may be effective in the treatment of hypertrophic scars/keloids. This review provides a detailed overview of the current literature on the RAS in skin, wound healing and scar formation and discusses the translational potential of targeting this hormonal system for treatment and prevention of hypertrophic scars and keloids.