The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
The other aspect of angiotensin or ACE2 I should say is that it gets rid of pro-oxidative products and it increases antioxidant products. So for instance, angiotensin II, and angiotensin (1-7), those are in balance and ACE2 tries to keep those in balance. But when ACE2 is knocked out by other SARS-CoV-2 or SARS 1, the amount of oxidative stress goes up dramatically. And what we see that that may play a role in terms of thrombosis.
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Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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So you have oxidative stress in the ACE2 receptors at the endothelium of the vasculature that causes inflammatory stress, oxidative stress, that causes thrombosis. And that's where that happens as well.