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FOXC1 Controls Smooth Muscle Cell Differentiation and Plasticity in Vascular Disease

Rykaczewska, Urszula ; Suur, Bianca E. ; Narayanan, Sampath ; Sundman, Sofija ; Auguste, Gaelle ; Zhao, Quanyi ; Zhang, Xiang ; Prasad, Inika ; Hedman, Åsa and Lengquist, Mariette , et al. (2026) In JACC: Basic to Translational Science 11(6).
Abstract

Smooth muscle cell–related transcription factors have been associated with coronary artery disease in large genome-wide association studies, increasing their translational value for therapeutic investigations. Our study shows for the first time that FOXC1 is a major transcriptional regulator in vascular injury and atherosclerotic lesions, causally implicated in the disease. Functionally, our data suggest that FOXC1 modulates smooth muscle cell activation vs quiescence by regulating key pathways involved in cell adhesion, cell cycle progression, and actin cytoskeleton organization. Further investigations should focus on elucidating the mechanistic basis of these regulatory effects and assessing whether this axis could be... (More)

Smooth muscle cell–related transcription factors have been associated with coronary artery disease in large genome-wide association studies, increasing their translational value for therapeutic investigations. Our study shows for the first time that FOXC1 is a major transcriptional regulator in vascular injury and atherosclerotic lesions, causally implicated in the disease. Functionally, our data suggest that FOXC1 modulates smooth muscle cell activation vs quiescence by regulating key pathways involved in cell adhesion, cell cycle progression, and actin cytoskeleton organization. Further investigations should focus on elucidating the mechanistic basis of these regulatory effects and assessing whether this axis could be pharmacologically targeted to promote lesion stability.

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organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
atherosclerosis, BiKE, FOXC1, smooth muscle cells
in
JACC: Basic to Translational Science
volume
11
issue
6
article number
101566
publisher
Elsevier
external identifiers
  • scopus:105038392425
  • pmid:42127570
ISSN
2452-302X
DOI
10.1016/j.jacbts.2026.101566
language
English
LU publication?
yes
id
42e148bd-662b-4336-a2a9-f573a38f4315
date added to LUP
2026-07-09 12:59:15
date last changed
2026-08-20 16:59:19
@article{42e148bd-662b-4336-a2a9-f573a38f4315,
  abstract     = {{<p>Smooth muscle cell–related transcription factors have been associated with coronary artery disease in large genome-wide association studies, increasing their translational value for therapeutic investigations. Our study shows for the first time that FOXC1 is a major transcriptional regulator in vascular injury and atherosclerotic lesions, causally implicated in the disease. Functionally, our data suggest that FOXC1 modulates smooth muscle cell activation vs quiescence by regulating key pathways involved in cell adhesion, cell cycle progression, and actin cytoskeleton organization. Further investigations should focus on elucidating the mechanistic basis of these regulatory effects and assessing whether this axis could be pharmacologically targeted to promote lesion stability.</p>}},
  author       = {{Rykaczewska, Urszula and Suur, Bianca E. and Narayanan, Sampath and Sundman, Sofija and Auguste, Gaelle and Zhao, Quanyi and Zhang, Xiang and Prasad, Inika and Hedman, Åsa and Lengquist, Mariette and Kronqvist, Malin and Swärd, Karl and Razuvaev, Anton and Mälarstig, Anders and Eriksson, Per and Miller, Clint and Quertermous, Thomas and Hedin, Ulf and Matic, Ljubica}},
  issn         = {{2452-302X}},
  keywords     = {{atherosclerosis; BiKE; FOXC1; smooth muscle cells}},
  language     = {{eng}},
  number       = {{6}},
  publisher    = {{Elsevier}},
  series       = {{JACC: Basic to Translational Science}},
  title        = {{FOXC1 Controls Smooth Muscle Cell Differentiation and Plasticity in Vascular Disease}},
  url          = {{http://dx.doi.org/10.1016/j.jacbts.2026.101566}},
  doi          = {{10.1016/j.jacbts.2026.101566}},
  volume       = {{11}},
  year         = {{2026}},
}