Nature Communications, 2021 · DOI: https://doi.org/10.1038/s41467-021-25585-5 · Published: September 21, 2021
The central nervous system (CNS) in adult mammals has limited regeneration capabilities due to scar tissue formation after lesions. While this scar tissue is important for containing damage, it also prevents axons from regenerating, leading to lasting functional deficits. This study reveals that a specific subset of perivascular cells, termed type A pericytes, are the primary source of scar-forming fibroblasts in various CNS lesions. This finding was consistent across mouse models of spinal cord injury, traumatic brain injury, stroke, and multiple sclerosis. The discovery of type A pericyte-derived fibrosis as a conserved mechanism presents a potential therapeutic target for enhancing recovery after CNS lesions. Understanding and modulating this process could pave the way for treatments aimed at improving axonal regeneration and functional outcomes.
Type A pericytes can be explored as a therapeutic target to improve recovery after central nervous system lesions.
Fibrotic scarring by a small subset of perivascular cells, defined as type A pericytes, is an evolutionarily conserved mechanism for scar formation in the CNS.
The extent of type A pericyte progeny located outside the vascular wall determines the magnitude of fibrotic ECM deposition after brain lesions.