Phagocytosis Of Wnt Inhibitor Sfrp4 By Late Wound Macrophages Drives Chronic Wnt Activity For Fibrot
- Thread starter pegasus2
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What does it mean for somone who doesn't have a phd in neuroscience?
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It means dick, you still have to bathe in antiandrogens to have a chance of keeping sh*t on your head. None of these studies result in any real options for anyone so unless you are just scientifically curious on how and why your follicles are getting raped, you're not really missing out on much by not reading them, IMO.
It means that too much Wnt activity late in wound healing prevents HF neogenesis. We've already seen that before, but this tells us a little more about the mechanisms involved. It's been theorized that the immune system is responsible for promoting scarring in adult wounds instead of regeneration. This gives us an idea of how that works. Practically there's not a whole lot you can do with this. Discontinuing Wnt agonists or adding SFRP4 around 16-22d after wounding might help promote regeneration over scarring. The timing around this is crucial. You need to upregulate Wnts early in wound healing, but later in wound healing it leads to fibrosis. Exactly where do you draw the line in humans with Androgenetic Alopecia. It's impossible to say. If you want neogenesis you either use some kind of shh agonist(SAG, fgf9, etc.), or perfectly time upregulating and downregulating Wnts, which is a difficult task.
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