Researchers identified NR4A1, a protein that acts as a natural brake on TGF-β (a growth factor that can cause excess collagen buildup and scarring). When they used small-molecule compounds to activate NR4A1 in mice, it successfully reduced fibrosis in skin, lungs, liver, and kidneys—suggesting a potential new approach to prevent unwanted scarring and tissue damage.

Scientists studied how NR4A1 controls TGF-β signaling in tissue repair. They examined both normal wound healing (where the body naturally turns off TGF-β) and fibrotic conditions (where it stays on), then tested whether activating NR4A1 with experimental compounds could stop excessive scarring in multiple organs in mice.

Funding not disclosed in abstract