Catecholaminergic neurons boost fibroblast osteogenic activity in keloid
fibroblasts. Therapeutic interventions targeting catecholamine biosynthesis or adrenergic innervation, and pharmacological inhibition or genetic ablation of ADRB1 effectively prevent keloid-like pathology in a rodent model. Our study provides the demonstration of neuronal-adrenergic signaling driving fibrotic/osteogenic matrix overproduction through TSN-mediated RNA trafficking, revealing therapeutic targets for keloid management.
Authors
- Fangzhou Lou (ORCID: https://orcid.org/0000-0002-7127-1743)
- Zhenyao Xu (ORCID: https://orcid.org/0000-0003-1039-2282)
- Honglin Wang (ORCID: https://orcid.org/0000-0001-6302-6927)
- Fengjiao Zhang (ORCID: https://orcid.org/0000-0003-2299-4256)
- Aie Xu (ORCID: https://orcid.org/0000-0001-6018-5965)
- Jihuan Liang
- Qili PENG (ORCID: https://orcid.org/0000-0001-6905-1074)
- Yang SUN
- Rui CHEN (ORCID: https://orcid.org/0009-0001-6741-1555)
- Xiaojie CAI (ORCID: https://orcid.org/0000-0001-7297-4865)
- Siyu Deng
Institutions
- Shanghai Jiao Tong University (CN)
- Renji Hospital (CN)
- Third People's Hospital of Hangzhou (CN)
- Shanghai First People's Hospital (CN)
Publication Details
- Journal
- Nature Communications
- Published
- 2026-05-09
- DOI
- https://doi.org/10.1038/s41467-026-72823-9
- Primary Topic
- Dermatologic Treatments and Research
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Natural Science Foundation of Shanghai
- National Natural Science Foundation of China
- Science and Technology Commission of Shanghai Municipality