Angiotensin-converting enzyme 2, the complement system, the kallikrein-kinin system, type-2 diabetes, interleukin-6, and their interactions regarding the complex COVID-19 pathophysiological crossroads.
Because of the current COVID-19-pandemic, the world is currently being held hostage in various lockdowns. ACE2 facilitates SARS-CoV-2 cell-entry, and is at the very center of several pathophysiological pathways regarding the RAAS, CS, KKS, T2DM, and IL-6. Their interactions with severe COVID-19 complications (e.g. ARDS and thrombosis), and potential therapeutic targets for pharmacological intervention, will be reviewed.
['Hoevenaar|Martijn|M|https://orcid.org/0000-0003-1906-703X', 'Goossens|Dolf|D|https://orcid.org/0000-0003-0417-991X', 'Roorda|Janne|J|https://orcid.org/0000-0002-6624-6666']
D000085962:Angiotensin-Converting Enzyme 2 D000086382:COVID-19 D003165:Complement System Proteins D003924:Diabetes Mellitus, Type 2 D006801:Humans D015850:Interleukin-6 D016234:Kallikrein-Kinin System D000086402:SARS-CoV-2
angiotensin-converting enzyme 2 complement kallikrein-kinin system diabetes interleukin-6 COVID-19 thrombosis renin angiotensin aldosterone system