**5. Conclusions**

The purpose of this review is to show the role of HMGB1 in DR. Many studies have demonstrated that DM, and then hyperglycemia, upregulate the expression of and increase in the levels of HMGB1. This situation activates several pathways and involves a large number of molecules, such as ERK, NF-κB, ICAM, RAGE, VEGF, and TLR. The final result is the activation and increase of inflammation, angiogenesis, oxidative stress, and, ultimately, retinal damage to the patients. At the same time, the involvement of this grea<sup>t</sup> number of molecules can provide a hint of new therapeutic approaches to be developed and studied.

**Author Contributions:** Conceptualization, M.N. and A.L.; writing—original draft preparation, M.A., L.A., and G.T.; writing—review and editing, M.N., M.A., L.A., and G.T.; supervision, A.L., R.P., and V.B. 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.
