LRM increases killing with nitric oxide which indu
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Posted On: 07/03/2022 8:56:29 PM
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LRM increases killing with nitric oxide which induces inflammation.
The beneficial effects of NOS in NASH are because of it's control of reactive oxygen species and it's regulation of mitochondrial dysfunction. NOS activates AMPK and downregulates mTORc1, both actions induce death in damaged mitochondria. Damaged mitochondria induce inflammation, NOS takes care of that. Leronlimab upregulates AMPK and downregulates mTORc1 and NOS may be one of the pathways it uses.
I have a previous post that goes into that in regards to IL-13, a1-antitrypsin and damaged mitochondria.
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Ran into something that may pertain to something I posted earlier. Another way leronlimab can help across a wide range of diseases.
A possible explanation - Mitochondria are cells that are essential in the conversion of glucose to energy. Excessive damage to mitochondria means less efficient usage of glucose and more storage to fat. a1-antitrypsin is protective of mitochondria.
IL-13 is increased in inflammatory states. IL-13 can significantly decrease amounts of a1-antitrypsin. CCR5 blockade downregulates IL-13 leading to an increase in a1-antitrypsin and protection of mitochondria.
I originally ran into a1-antitrypsin while looking at Covid caused mitochondria damage. What's interesting is that low levels of a1-antitrypsin are also implicated in liver disease and pulmonary inflammation. No one seems to have made the connection between CCR5 blockade, IL-13, a1-antitrypsin and mediation of a variety of diseases.
A possible explanation - Mitochondria are cells that are essential in the conversion of glucose to energy. Excessive damage to mitochondria means less efficient usage of glucose and more storage to fat. a1-antitrypsin is protective of mitochondria.
IL-13 is increased in inflammatory states. IL-13 can significantly decrease amounts of a1-antitrypsin. CCR5 blockade downregulates IL-13 leading to an increase in a1-antitrypsin and protection of mitochondria.
I originally ran into a1-antitrypsin while looking at Covid caused mitochondria damage. What's interesting is that low levels of a1-antitrypsin are also implicated in liver disease and pulmonary inflammation. No one seems to have made the connection between CCR5 blockade, IL-13, a1-antitrypsin and mediation of a variety of diseases.
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