Cellular aging prevents fibrosis during wound healing

Cellular senescence is thought to be a tumour suppressive mechanism, but there are few studies demonstrating a role for cellular senescence in diseases other than cancer. Work presented in Nature Cell Biology now suggests that cellular senescence, mediated by the protein CCN1, prevents the formation of excess tissue during wound healing.

Cellular senescence is when cells remain viable but lose the ability to divide. Jun and Lau find that in mice senescent cells appear in the granulation tissue ― the soft connective tissue that forms in the wound during healing. In mice lacking functional CCN1, fewer senescent cells appear. The authors therefore conclude that CCN1 mediates senescence, and they go on to characterize the mechanism by which CCN1 exerts this function.

They also find that fibrosis ― the formation of excess fibrous tissue ― is increased in wounds of mice lacking functional CCN1. Conversely, application of CCN1 protein to the wound induces cell senescence and prevents fibrosis in these mice.

Fibrosis is associated with many diseases. These data reinforce the importance of senescence as an antifibrotic mechanism.