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. 2020 Dec 10;11:532. doi: 10.1186/s13287-020-02026-6

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© The Author(s) 2020

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 9 — A scheme depicting a putative mechanism for the anti-hypertrophic effects caused by miR-218 in MSC and activation of a feedback loop due to concomitant effects on inhibitors of WNT/β-catenin signaling. MiR-218 targets hypertrophy-related mRNAs: MEF2C and its downstream targets, COL10A1 and IBSP, leading to attenuation of the hypertrophic phenotype. Among the other targets of miR-218, there is RUNX2, a transcription factor regulating expression of COL10A1 and ALPL. However, accumulation of β-catenin due to concomitant targeting of WNT signaling inhibitors activates a feedback loop that counteracts the anti-hypertrophic alterations. Arrows indicate directions of expression regulation: red—downregulation, green—upregulation