"ACE2 thereby helps to protect multiple tissues such as the lung, blood vessels, heart, or kidney, and inactivation of ACE2 results in severe disease pathologies in these organs including diabetic nephropathies. ACE2 has also been identifying as the critical receptor for the Spike proteins of SARS-CoV and SARS-CoV2 and is intricately involved in SARS and COVID-19 pathogenesis."
Yes, Jennifer. Dr. Josef Penninger has tried it. Soluble ACE2 works. Reduces viral load 1000 - 5000 times.36 min mark in video.https://t.co/Mrd8MqhrU9
— Walter M Chesnut (@Parsifaler) November 11, 2021
This video was released on February 3, 2021.
ACE2 Receptors protect against heart disease. ACE2 is heavily expressed in the lungs, and we didn't know what it was doing. Severe inflammation and increased vascular permeability in ACE2 knockout mice in ARDS, or Acute Respiratory Distress Syndrome.
Soluble angiotensin-converting enzyme 2 (sACE2) could be a therapeutic option to treat coronavirus disease 2019 (COVID-19) infection. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) utilizes ACE2 receptors on cell surfaces to gain intracellular entry, making them an ideal target for therapy. High-affinity variants of sACE2, engineered using high-throughput mutagenesis, are capable of neutralizing COVID-19 infection as decoy receptors. These variants compete with native ACE2 present on cells by binding with spike (S) protein of SARS-CoV-2, making native ACE2 on cell surfaces available to convert angiotensin II to angiotensin-1,7, thus alleviating the exaggerated inflammatory response associated with COVID-19 infection. This article explores the use of sACE2 as potential therapy for COVID-19 infection.
At the 8:51 mark, he cites Yumiko Imai's findings of the function of ACE2 receptors, and you can check out that discussion here. Besides ACE2 receptors, other receptors were reported in cell lines, like the cell membrane protein, L-Sign/CLEC4M. But he learned that the ACE2 receptor is essential for Coronavirus infection; no ACE2 receptor, no COVID. Check this out,
SARS infection downregulates, lowers the rate or level of, ACE2 expression in the lungs. The ACE2 receptor disappeared in the lungs and in the heart. The virus binds to ACE2 and takes it with it into the cell, where the ACE2 is being degraded. The virus more or less creates an ACE2 mutant background. And this was interesting becauase it gave us a molecular understanding of how the SARS-CoV-2 became such a killer virus because of various injuries in the lung.
14:07 ACE2 as therapy for acute lung injury. If this is the acase, then we can create an enzyme replacement therapy.
Biotech company in Vienna, Apeiron Biologics, developed a soluble Recombinant Angiotensin Converting Enzyme System 2 molecule APN01 for therapeutic use against lung failure. Lung failure is an end stage of many diseases-sepsis, gastric aspiration, the Spanish Flu, bird flu, bioterrorist agents. This moleculre actually went through 89 humans already, healthy volunteers in Phase I trials and in Phase II trials. Also into people who had lung disease.
Just to show you there's some that actually developed with Glaxo-Smith Kline with older rights belong to us--to us meaning this biotech in Vienna, Apeiron Biologics. So Glaxo-Smith Kline is not involved with this anymore.
It's a key regulator of the Renin-Angiotensin System, which in turn regulates blood pressure.
