Ahmed-Belkacem, R., Debart, F
When estrogen declines, so does one of your bodys natural shields against oxidative stress
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The title for Figure 4 should be reconsidered as the term "mutually opposite signal modulation" is unclear and/or does not reflect the description to follow. Response: We have replaced the term mutually opposite signal modulation with: amplification of MC3R signaling and attenuation of GHSR1a signaling For Figure 5, the figure legend should clarified if 5-HT2c-GHSR1a dimerization produces reduced Ca++ accumulation with (as appears to be implied by the figure) or without ligand for each receptor. Response: To make it clearer that the 5-HT2C ligand is not required, while the ghrelin ligand is, we have changed the description to read: When dimerized with 5-HT2C, GHSR1a displays a 65% reduction in ghrelin-induced Ca2+ accumulation, with this effect not requiring the presence of a 5-HT2C ligand. Reviewer #2: The review includes an excellent explanation of GSHR1a dimerization with other receptors at the cellular and molecular level and also does a good job of explaining technical aspects of this type of work
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Hepatic miRNA let-7b-5p is a potential reason why TGF-RII is pro-fibrotic, as let-7b-5p is much higher in MASLD patients when TGF- signaling is enhanced, whereas let-7b-5p is reduced in TGF-RII KO in hepatocytes (Zhao et al
