An ERK-Dependent Molecular Switch Antagonizes Fibrosis and Promotes Regeneration in Spiny Mice

The study "An ERK-dependent molecular switch antagonizes fibrosis and promotes regeneration in spiny mice (Acomys)" found that high levels of extracellular signal-regulated kinase (ERK) activity are crucial for complex tissue regeneration. This was observed in spiny mice, which naturally regenerate skin and complex musculoskeletal tissues. When ERK was inhibited, the mice's tissue regeneration shifted towards fibrotic repair. The study also identified fibroblast growth factor and ErbB signaling as upstream ERK regulators of regeneration. Activating ERK in scar-prone injuries induced a pro-regenerative response, including cell proliferation, extracellular matrix remodeling, and hair follicle neogenesis. This suggests potential ways to redirect fibrotic repair towards regenerative healing in adult mammals.