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Contribution of fibroblast dysregulation to arteriolar fibrosis and stenosis in CADASIL

Determine whether fibroblast dysregulation is a causal contributor to arteriolar fibrosis and stenosis in CADASIL and whether such dysregulation could be corrected by gene editing.

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Background

Arteriolar stenosis and vessel wall fibrosis are common in CADASIL, but the cellular drivers are not fully resolved. While VSMC pathology is central, the potential role of fibroblast dysregulation in driving fibrosis remains uncertain.

Establishing the contribution of fibroblasts would clarify therapeutic targets and whether fibroblast-directed gene editing could mitigate vascular remodeling in CADASIL.

References

Whether these symptoms can be attributed to fibroblast dysregulation which could be resolved through gene editing is unknown, although edited fibroblasts may not resolve VSMC cell death seen in CADASIL models and patient pathology [23,54].

— Cerebral Autosomal Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL): Immunotherapy and Cell Therapy approaches (2506.09293 - Haile et al., 10 Jun 2025) in CADASIL as a Candidate for Cell and Gene Therapy