Deficiency of <i>ZC3HC1</i> Modulates Vascular Smooth Muscle Cell Phenotype and Increases Neointima Formation
ZC3HC1 acts as a dosage-sensitive modulator of SMC phenotype. Partial reduction promotes a synthetic, proliferative state and neointima formation, while complete loss induces a quiescent phenotype. These findings provide mechanistic insight into the paradoxical clinical associations of the rs11556924-T allele and identify ZC3HC1 as a potential target for modulating SMC phenotypes in vascular disease.
Authors
- Heribert Schunkert (ORCID: https://orcid.org/0000-0001-6428-3001)
- Thorsten Kessler (ORCID: https://orcid.org/0000-0003-3326-1621)
- Zouhair Aherrahrou (ORCID: https://orcid.org/0000-0002-1241-8733)
- Rédouane Aherrahrou (ORCID: https://orcid.org/0000-0001-8148-9554)
- Xiaoke Yin (ORCID: https://orcid.org/0000-0002-5172-0935)
- Tobias Reinberger (ORCID: https://orcid.org/0000-0002-6237-0803)
- Julia Werner (ORCID: https://orcid.org/0000-0002-4374-5374)
- Jaafar Al-Hasani
- Miriam Otto
- Maria Loreto Munoz-Venegas
- Manuel Mayr
- Mete Civelek
Institutions
- University of California, Los Angeles (US)
- University of Eastern Finland (FI)
- Augusta University (US)
- British Heart Foundation (GB)
- Lung Institute (US)
- Precision for Medicine (United States) (US)
- German Centre for Cardiovascular Research (DE)
- Deutsches Herzzentrum München (DE)
- Heartland Alliance (US)
- Saarland University (DE)
- University of Lübeck (DE)
Publication Details
- Journal
- Arteriosclerosis Thrombosis and Vascular Biology
- Published
- 2026-03-12
- DOI
- https://doi.org/10.1161/atvbaha.125.323659
- Primary Topic
- Angiogenesis and VEGF in Cancer
- Type
- article
- Field-Weighted Citation Impact
- 0.00