**5. Conclusions**

Our study demonstrated that fenofibrate inhibited ROS accumulation, diminished mitochondrial dysfunction, as well as modulating several apoptotic and survival signal pathways in oxidative stress-induced RF/6A cells. The mechanism of action could be through enhancing Trxs expression and suppressing Ask-1 activity, which in turn inhibited the subsequent apoptotic signaling pathways. The anti-oxidative and anti-apoptotic beneficial effects of fenofibrate identified in this study may provide new insights into the design of therapeutic strategies concerning the imbalance between pro-apoptotic and survival pathways induced by oxidative stress in DR.

**Author Contributions:** Conceptualization, Y.-J.H., C.-W.L., S.-L.C., W.-S.Y. and C.-H.Y.; Data curation, Y.-J.H. and S.-L.C.; Formal analysis, Y.-J.H., C.-W.L. and C.-H.Y.; Funding acquisition, C.-M.Y. and C.-H.Y.; Investigation, Y.-J.H., C.-W.L., S.-L.C. and C.-H.Y.; Methodology, Y.-J.H., C.-W.L., S.-L.C., W.-S.Y. and C.-H.Y.; Project administration, W.-S.Y., C.-M.Y. and C.-H.Y.; Resources, C.-W.L., W.-S.Y., C.-M.Y. and C.-H.Y.; Software, C.-M.Y.; Supervision, W.-S.Y., C.-M.Y. and C.-H.Y.; Validation, Y.-J.H. and C.-W.L.; Visualization, Y.-J.H., C.-W.L. and S.-L.C.; Writing—original draft, Y.-J.H., C.-W.L. and S.-L.C.; Writing—review & editing, C.-M.Y. and C.-H.Y. All authors have read and agreed to the published version of the manuscript.

**Funding:** This research received no external funding.

**Conflicts of Interest:** The authors declare no conflict of interest.
