Discussion of rationale for targeting CCR5 in fatt

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:

Quote:

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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

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Simplest possible explanation:

CCL5 bad for liver.
Leronlimab block CCL5 from making liver turn fatty and fibrous.

We hope.