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Posted On: 12/13/2021 1:39:38 PM
Post# of 148925
Discussion of rationale for targeting CCR5 in fatty liver:
https://www.tandfonline.com/doi/full/10.1080/...20.1718106
https://www.sciencedirect.com/science/article...4416301773
Picture says a thousand words:
Blocking CCR5 keeps the macrophages away and keeps the myofibroblastasts from activating and forming collagen fibers that stiffen the liver.
The other paper says:
Simplest possible explanation:
CCL5 bad for liver.
Leronlimab block CCL5 from making liver turn fatty and fibrous.
We hope.
https://www.tandfonline.com/doi/full/10.1080/...20.1718106
https://www.sciencedirect.com/science/article...4416301773
Picture says a thousand words:
Blocking CCR5 keeps the macrophages away and keeps the myofibroblastasts from activating and forming collagen fibers that stiffen the liver.
The other paper says:
Quote:.
In the current study, we were endeavored to characterize a proinflammatory cytokine, CCL5, as a major contributor for fibrosis in NAFLD. The results showed that CCL5 was highly expressed in fatty liver and NASH patients. In NAFLD rats induced by 8-week-HFD, CCL5 and its receptor, CCR5, were significantly up-regulated and liver fibrosis exclusively occurred in this group. In addition, we showed that hepatocytes are the major source contributing to this CCL5 elevation. Interestingly, a CCL5 inhibitor Met-CCL5, significantly decreased liver fibrosis but not hepatic steatosis
Simplest possible explanation:
CCL5 bad for liver.
Leronlimab block CCL5 from making liver turn fatty and fibrous.
We hope.
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