Smooth Muscle Cell‐Derived Fibronectin Promotes an Atheroprotective Smooth Muscle Cell Phenotype Associated With Altered NO‐cGMP Signaling
SMC-derived Fn1 promotes plaque stability through suppression of SMC phenotypes with low alpha smooth muscle actin and collagen expression. This atheroprotective effect might be mediated, at least in part, by a crosstalk between Fn1 and the NO-cGMP axis in SMCs. Our study identifies a mechanistic link between 2 coronary artery disease risk genes, Fn1 and NO-GC, which explains how the extracellular matrix regulates SMC phenotype and plaque stability.
Authors
- Jacob Fog Bentzon (ORCID: https://orcid.org/0000-0002-3020-5002)
- Moritz Lehners (ORCID: https://orcid.org/0000-0002-3841-3930)
- Susanne C. Feil (ORCID: https://orcid.org/0000-0003-2148-8773)
- Jennifer R. Kiesel
- Andreas Peter (ORCID: https://orcid.org/0000-0001-5732-2287)
- Robert Feil (ORCID: https://orcid.org/0000-0002-7335-4841)
- Daniel Morales‐Cano (ORCID: https://orcid.org/0000-0002-1692-4633)
- Malte Roeßing (ORCID: https://orcid.org/0009-0003-0944-0862)
- Maria T. K. Zaldivia
Institutions
- Aarhus University (DK)
- Aarhus University Hospital (DK)
- Spanish National Centre for Cardiovascular Research (ES)
- University Children's Hospital Tübingen (DE)
- University of Tübingen (DE)
Publication Details
- Journal
- Journal of the American Heart Association
- Published
- 2025-05-29
- DOI
- https://doi.org/10.1161/jaha.124.040395
- Citations
- 2
- Primary Topic
- Cell Adhesion Molecules Research
- Type
- article
- Field-Weighted Citation Impact
- 3.24