It's not clear to me if any of this has been confirmed to a good degree (meaning in terms of actual mechanisms), but in the realm of hypotheses, a fairly cited paper indeed links ACE2 deficiency (caused by a combination of genetic and viral factors) with thrombotic processes:
Clinical reports of patients infected with SARS-CoV-2 show that several features associated with infection and severity of the disease (i.e., older age, hypertension, diabetes, cardiovascular disease) share a variable degree of ACE2 deficiency. We suggest that ACE2 down-regulation induced by viral invasion may be especially detrimental in people with baseline ACE2 deficiency associated with the above conditions. The additional ACE2 deficiency after viral invasion might amplify the dysregulation between the ‘adverse’ ACE→Angiotensin II→AT1 receptor axis and the ‘protective’ ACE2→Angiotensin1-7→Mas receptor axis. In the lungs, such dysregulation would favor the progression of inflammatory and thrombotic processes triggered by local angiotensin II hyperactivity unopposed by angiotensin1-7.
But even this paper notes that there are obviously competing or concurrent mechanisms, at least in the lungs, responsible for lung symptoms:
the damage of pneumocytes type II due to the binding of coronavirus to ACE2 receptors is devastating for at least three reasons: 1) local unopposed ACE→Angiotensin II→AT1 receptor axis over-activity; 2) reduced production of alveolar surfactant by injured pneumocytes type II leading to reduced lung elasticity; 3) reduced repair of pneumocytes type I leading to impaired gas exchanges and fibrosis.
There's another paper (citing the above) on "(micro)thrombosis" in Covid-19 patients, but again it does little more than
repeat that hypothesis, although it does mention a couple of experiments:
human blood vessel organoids, which closely resemble human capillaries, contain viral RNA after exposure to COVID-19 in vitro. Strikingly, the application of human recombinant soluble ACE-2 markedly inhibited viral infection in human capillary organoids, pointing to a direct role for endothelial ACE-2 in viral uptake in blood vessels. Intriguingly, the uptake of SARS-CoV-2 into cells is associated with the downregulation of ACE-2 expression. This appears to play an important role in promoting a proinflammatory and prothrombotic milieu since ACE-2 plays a pivotal role in regulating the RAS (renin-angiotensin system), by degrading angiotensin II to angiotensin 1–7. While angiotensin II induces vasoconstriction and promotes a proinflammatory/prothrombotic phenotype, angiotensin 1–7 opposes these effects via binding to the MAS receptor, which is widely expressed including on endothelial cells and platelets.