Major impact exists in susceptibility and severity outcomes of SARS-CoV-2 ( severe-acute-respiratory-syndrome-coronavirus-2) infection in individuals with comorbidities including hypertension, diabetes and lung diseases; It is due to increased expression of virus entry receptor ACE2 (angiotensin-converting enzyme 2) on the surface of host cells among those patients. Furthermore, these conditions appear to track closely with advancing age, which is emerging as the strongest predictor of coronavirus disease 2019 (Covid-19)–related death. Indeed, SARS-Cov-2 infection in severe cases is mainly due to dysregulated and excessive innate immune host response.
Endothelial dysfunction (ED) appears to be the common linkage between these coexisting conditions. However, whether and how ED relates or has contributed to the adverse health outcomes observed needs to be discussed. Understanding the baseline mechanisms involved during this infection is key to managing disease and developing additional protective strategies.
There is no effective treatment for Covid-19. The infectious disease has a rapid pace with deadly outbreak and vaccine development is a lengthy process.
Clarifying the common features shared by the Covid-19 most affected phenotypes and the underlying mechanisms is of the greatest importance for cardiovascular protection before infection as well as for managing severe outcomes and reduced mortality.
Recent advances understanding the immune system imbalanced response during Covid-19 infection evokes new ideas about therapeutic interventions.
We expect authors to share important information on the following topics:
1) Does exercise training modulate ACE-2 expression on cells?
2) Diabetes and ACE-2 expression: inflammation and immune response.
3) Are major Covid-19 outcomes in diabetic patients due to glycation micro and macrovascular complications?
4) Shear stress and ACE-2 receptor.
5) How does Covid-19 affect immunity and inflammation on young versus aging patients?
6) Coagulation, thrombosis and homeostasis.
7) Molecular basis in endothelial (cell) dysfunction.
8) Microcirculatory dysfunction.
9) Endothelial dysfunction: inflammation and immune response (during viral infection).
10) Vasoactive factors and hypertension.
11) Vascular oxidative stress and redox regulation of vasculature.
12) Redox regulation of immune response.
13) Pro-protein convertases in CAD and Covid-19: Furin-like cleavage sites discovered in SARS-CoV-2 spike proteins.
14) Viral particle assembly and mutations explained.
15) Insomnia, Heart disease and Covid-19.
16) Stem cells treatment for Covid-19.
Major impact exists in susceptibility and severity outcomes of SARS-CoV-2 ( severe-acute-respiratory-syndrome-coronavirus-2) infection in individuals with comorbidities including hypertension, diabetes and lung diseases; It is due to increased expression of virus entry receptor ACE2 (angiotensin-converting enzyme 2) on the surface of host cells among those patients. Furthermore, these conditions appear to track closely with advancing age, which is emerging as the strongest predictor of coronavirus disease 2019 (Covid-19)–related death. Indeed, SARS-Cov-2 infection in severe cases is mainly due to dysregulated and excessive innate immune host response.
Endothelial dysfunction (ED) appears to be the common linkage between these coexisting conditions. However, whether and how ED relates or has contributed to the adverse health outcomes observed needs to be discussed. Understanding the baseline mechanisms involved during this infection is key to managing disease and developing additional protective strategies.
There is no effective treatment for Covid-19. The infectious disease has a rapid pace with deadly outbreak and vaccine development is a lengthy process.
Clarifying the common features shared by the Covid-19 most affected phenotypes and the underlying mechanisms is of the greatest importance for cardiovascular protection before infection as well as for managing severe outcomes and reduced mortality.
Recent advances understanding the immune system imbalanced response during Covid-19 infection evokes new ideas about therapeutic interventions.
We expect authors to share important information on the following topics:
1) Does exercise training modulate ACE-2 expression on cells?
2) Diabetes and ACE-2 expression: inflammation and immune response.
3) Are major Covid-19 outcomes in diabetic patients due to glycation micro and macrovascular complications?
4) Shear stress and ACE-2 receptor.
5) How does Covid-19 affect immunity and inflammation on young versus aging patients?
6) Coagulation, thrombosis and homeostasis.
7) Molecular basis in endothelial (cell) dysfunction.
8) Microcirculatory dysfunction.
9) Endothelial dysfunction: inflammation and immune response (during viral infection).
10) Vasoactive factors and hypertension.
11) Vascular oxidative stress and redox regulation of vasculature.
12) Redox regulation of immune response.
13) Pro-protein convertases in CAD and Covid-19: Furin-like cleavage sites discovered in SARS-CoV-2 spike proteins.
14) Viral particle assembly and mutations explained.
15) Insomnia, Heart disease and Covid-19.
16) Stem cells treatment for Covid-19.
