I'm not a medical professional so Idk. Honestly, I've only just begun to research all of this too, so forgive me if I get details wrong. All I understand is simply this.
According to some theories surrounding c19 but the s protein specifically, there is some effect it has on the renin angiotensin system.
As I understand from the renin angiotensin system, the renin combines with angiotensinogen to form angiotensin-1 where it then further combines with ACE (not ACE-2 yet) to make angiotensin-2 which basically increases salt and fluid retention or w/e after interacting with the adr enaIgIand and also affecting VASOCONSTRlCTlON which is needed to help regulate movement in our circulatory system that mimics peristalsis. This eventually goes to the ACE2 where sheddase performs a proteolytic cIeavage on the metalloprotein which increases concentrations of ACE2 until it forms angiotensin-1-7 from angiotensin-2 which helps VASODlLATlON.
Question I have is this. How does the modified s protein work? When they say the modified one interacts with ACE-2, does that mean it's performing cIeavage itself or do the modifications to it kind of make ACE-2 think it's been activated without increasing concentrations of ACE-2, affecting the homeostasis between angiotensin-2 and angiotensin-1-7 and thereby causing a disproportionate level of VASOCONSTRlCTlON and VASODlLATlON? Because, as I understand it, there's already quite a number of treatment options available RIGHT NOW that help regulate angiotensin.
PLEASE SHARE THIS WITH A BASED DOCTOR.
I'm not a medical professional so Idk. Honestly, I've only just begun to research all of this too, so forgive me if I get details wrong. All I understand is simply this.
According to some theories surrounding c19 but the s protein specifically, there is some effect it has on the renin angiotensin system.
As I understand from the renin angiotensin system, the renin combines with angiotensinogen to form angiotensin-1 where it then further combines with ACE (not ACE-2 yet) to make angiotensin-2 which basically increases salt and fluid retention or w/e after interacting with the adr enaIgIand and also affecting VASOCONSTRlCTlON. This eventually goes to the ACE2 where sheddase performs a proteolytic cIeavage on the metalloprotein which increases concentrations of ACE2 until it forms angiotensin-1-7 from angiotensin-2 which helps VASODlLATlON.
Question I have is this. How does the modified s protein work? When they say the modified one interacts with ACE-2, does that mean it's performing cIeavage itself or do the modifications to it kind of make ACE-2 think it's been activated without increasing concentrations of ACE-2, affecting the homeostasis between angiotensin-2 and angiotensin-1-7 and thereby causing a disproportionate level of VASOCONSTRlCTlON and VASODlLATlON? Because, as I understand it, there's already quite a number of treatment options available RIGHT NOW that help regulate angiotensin.
PLEASE SHARE THIS WITH A BASED DOCTOR.