>>12186521>medium.com Anon do yourself a favor and use reputable sources. Here is a good article written in simple language:
https://www.thelancet.com/action/showPdf?pii=S2352-3964%2820%2930282-6Basically there are two different theories that kind of contradict each other:
what your article is saying is there is a *theory* that SARS upregulates ACE2 because it binds to ACE2. So theory is that an increased number of ACE2 makes it easier for SARS to spread into other organs. On the other hand, ACE2 are the "good guys" since they counter some negative effects caused by ACE. So the other *theory* is that SARS actually downregulates ACE2 so it no longer counters ACE. ACE is known to produce another group of "bad guys": angiotensin II which it breaks into angiotensin (1-9), a super evil guy responsible for high blood pressure and other bad things: it binds to AT1R and activativates really bad and harmful pathways. ACE2 on the other hand breaks angiotensin II into a good guy angiotensin (1-7) which binds to AT2R and activates the "good", protective pathways that counter AT1R. Long story short ACE2 is good for you is ACE is bad for you and thats what ACE inhibitors do that are used to treat high blood pressure.
That said, this is strictly in the context of RAS and has nothing to do with bradykinin storms. But since your article is based on the Bradykinin hypothesis, it is about a totally different system (KKS) and there is a complex interaction between RAS and KKS pathways. The article from lancet that I linked talks about both. Yet it insists that ARDS is linked to
*decreased* levels of ACE2 which implicates a loss of ACE2 protective effects. It also states that there is no evidence that ACE blockers prescribed for high blood pressure increase susceptibility to infection. For tl;dr you can read Summary at the bottom.
I also would like to point out that unlike RAS, KKS and this whole bradykinin stuff is very poorly understood due to insufficient research.
