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. 2016 Jul 18;6:29884. doi: 10.1038/srep29884

Figure 7. The working hypothesis of AcSDKP-mediated anti-fibrotic program through anti-fibrotic miRs crosstalk.

Figure 7

AcSDKP could induce both miR-29s and miR-let-7s. Elevated level of miR-let-7s suppressed TGF-β associated signaling, which concomitantly induced the miR-29s gene expression. Elevated levels of miR-29s inhibit of IFN-γ, which in turn activates FGFR1 phosphorylation, which was essential for miR-let-7 induction. AcSDKP could regulate such anti-fibrotic miRs crosstalk.