Inflammation Regulates the Multi-Step Process of Retinal Regeneration in Zebrafish

The ability to regenerate tissues varies between species and between tissues within a species. Mammals have a limited ability to regenerate tissues, whereas zebrafish possess the ability to regenerate almost all tissues and organs, including fin, heart, kidney, brain, and retina. In the zebrafish brain, injury and cell death activate complex signaling networks that stimulate radial glia to reprogram into neural stem-like cells that repair the injury. In the retina, a popular model for investigating neuronal regeneration, Muller glia, radial glia unique to the retina, reprogram into stem-like cells and undergo a single asymmetric division to generate multi-potent retinal progenitors. Muller glia-derived progenitors then divide rapidly, numerically matching the magnitude of the cell death, and differentiate into the ablated neurons. Emerging evidence reveals that inflammation plays an essential role in this multi-step process of retinal regeneration. This review summarizes the current knowledge of the inflammatory events during retinal regeneration and highlights the mechanisms whereby inflammatory molecules regulate the quiescence and division of Muller glia, the proliferation of Muller glia-derived progenitors and the survival of regenerated neurons.

Automated summary

Zebrafish have remarkable regenerative potential, with the ability to regenerate almost all tissues and organs. In the zebrafish brain and retina, radial glia can reprogram into stem-like cells to repair damaged tissues. Inflammation plays a crucial role in regulating the process of retinal regeneration, affecting the quiescence, division, and survival of the cells involved.