New Study Identifies Molecular Pathway to Reduce Fibrotic Scarring After Spinal Cord Injury

A new study published in Burns & Trauma on March 12, 2026, reveals a molecular pathway that drives fibrotic scarring after spinal cord injury (SCI) and demonstrates that targeting key components of this pathway can improve functional recovery in mice. The research, conducted by a team from multiple institutions in China, identifies the c-Jun–Irf8–CD36 axis as a central mechanism in the formation of dense scar tissue that blocks nerve regeneration.

Fibrotic scarring is a major obstacle to spinal cord repair. While initial scar formation helps stabilize the wound, excessive fibrosis later creates a physical and biochemical barrier that prevents axon regrowth. Current clinical treatments, such as decompression surgery and anti-inflammatory drugs, focus on limiting secondary damage rather than modifying the scar itself. This study offers a more targeted approach: reshaping the scar to be less inhibitory.

Using single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics, the researchers mapped CD36 expression after SCI and found it concentrated in lesion scars, particularly in specific fibroblast subpopulations associated with fibrotic progression. They then tested two inhibitors in mouse SCI models: salvianolic acid B (SAB), which targets CD36, and T5224, an inhibitor of the transcription factor c-Jun. Both treatments reduced fibrotic scar formation, enhanced angiogenesis, supported axonal regrowth, and improved hindlimb motor function.

The study further elucidated the mechanism: c-Jun activates Irf8, which then promotes CD36 transcription, establishing a signaling cascade. CUT&Tag and dual-luciferase reporter assays confirmed this regulatory connection. Multi-omic analyses showed that T5224 selectively restrained the abnormal expansion of CD36-positive fibroblast subclusters and shifted their transcriptional state toward a less fibrotic, more repair-permissive phenotype.

The authors suggest that the goal should not be to eliminate scar tissue entirely but to modulate it at the right stage—preserving its early protective role while preventing the formation of a long-lasting fibrotic wall. Because both CD36 and c-Jun are pharmacologically targetable, these findings provide a foundation for developing stage-adapted therapies for SCI. The research also highlights how advanced techniques like scRNA-seq and spatial transcriptomics can reveal cellular dynamics and treatment effects at high resolution.

Further validation in larger animal models and preclinical systems is needed before translation to human therapy. The study was supported by several Chinese funding agencies, including the National Major Project of Research and Development and the National Natural Science Foundation of China. The full article is available at https://doi.org/10.1093/burnst/tkag020.

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