Noggin is a glycosylated protein that can act as an inhibitor of bone morphogenetic protein (BMP) and has been shown in animal studies to improve functional recovery after spinal cord injury (SCI). Its mechanism of action promotes the regeneration and repair of damaged spinal cord tissue by regulating the differentiation and growth of glial cells and regulates the interaction between neurons and glial cells. However, very few studies on endogenous Noggin have been reported, and the available studies are limited to the therapeutic effects of exogenous Noggin. Therefore, we explored the expression and role of endogenous Noggin after SCI using Noggin-GFP transgenic mice and Nogginlox/lox; Nestin-cre conditional knockout mice. The results showed that Noggin was upregulated in the spinal cord after SCI, mainly in reactive astrocytes. In addition, endogenous Noggin was found to play a key role in regulating SCI responses, promoting GFAP expression of astrocytes, and improving functional recovery. These findings suggest that Noggin may be a therapeutic target for controlling glial scar formation after SCI.