Letter to the editor regarding the article “knocking-down long non-coding RNA LINC01094 prohibits chondrocyte apoptosis via regulating microRNA-577/metal-regulatory transcription factor 1 axis”

Dear Editor,

We have recently been very interested and discussed in depth an article entitled “Knocking-down long non-coding RNA LINC01094 prohibits chondrocyte apoptosis via regulating microRNA-577/metal-regulatory transcription factor 1 axis”. ¹ This study indicated the role of LINC01094 in the pathogenesis of osteoarthritis (OA). At the same time, its detailed action mechanism was also uncovered, namely LINC01094 knocking-down synergistic interaction with miR-577/MTF1 pathway to protect against OA development. We are very grateful to the authors for their contributions to this study, but the following issues still need to be discussed together.

First, Xie et al. ² concluded that maintenance of articular cartilage requires PTEN inhibition of the AKT signaling pathway, and that persistent AKT signaling in articular chondrocytes induces osteoarthritis through oxidative stress induced senescence in mice. LINC01094 down-regulated PTEN expression and further up-regulated the AKT pathway. ³ So the inhibitory effect of knockdown of LINC01094 on chondrocyte apoptosis may also be related to the PTEN/AKT pathway. In this study, the authors did not consider the effect of LINC01094 on the PTEN/AKT pathway so that it may have some infuence on the study results.

It was found that HMGB1 was able to regulate apoptosis-related signaling pathways involved in the progression of OA, and the related signaling pathways mediated by it were able to increase the rate of chondrocyte apoptosis to a certain extent. ⁴ LINC01094 promotes the expression of HMGB1. ⁵ Therefore, the authors should consider the effect of this factor on the experimental results. Finally, we would like to thank the authors again for their contribution. This work is of great help in the treatment of osteoarthritis.