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Peer-reviewedCC BYInternational journal of molecular sciences

Myf5 Progenitors Define the Lineage Identity of Somitic Vascular Smooth Muscle Cells.

  • Donghua Hu1
  • Kun Chen2,3
  • Xifeng Chang2
  • Xi Hu2,3
  • Hongjin Chen2
  • Xingrong Zhai2
  • Xinkai Qu2
  • Lei Fu3
  • Cheng-Chao Ruan1
  • Kailei Shi2
  1. 1Shanghai Key Laboratory of Bioactive Small Molecules, Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai 200032, China.
  2. 2Department of Cardiology, Huadong Hospital, Fudan University, Shanghai 200040, China.
  3. 3Shanghai Key Laboratory of Clinical Geriatric Medicine, Shanghai Institute of Geriatrics and Gerontology, Huadong Hospital, Fudan University, Shanghai 200040, China.
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Abstract

Vascular smooth muscle cell (VSMC) heterogeneity drives region-specific aortic pathologies, yet the roles of somite-derived lineages remain unclear. Utilizing Myf5 and MyoD lineage tracing alongside a smooth muscle-specific Myf5 conditional knockout model, we show that Myf5-derived cells selectively populate the thoracic aortic media, whereas the MyoD lineage completely spares large arteries. Early embryonic Myf5 deletion suppressed embryonic VSMC proliferation and downregulated α-SMA, reduced the synthesis of elastic, establishing its necessity in aortic morphogenesis. Upon in vitro ox-LDL challenge and calcification induction, the non-Myf5 lineage primarily drives excessive proliferation and osteogenic transdifferentiation, whereas Myf5 lineage VSMCs exhibit remarkable phenotypic stability and resistance to PDGF-BB-induced dedifferentiation compared to their non-Myf5 counterparts. Collectively, our findings demonstrate a strict lineage divergence between Myf5 and MyoD, suggesting that Myf5 lineage cells play an important role in maintaining aortic integrity, and uncover a lineage-imprinted plasticity that explains regional vascular heterogeneity.

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Cite

BibTeXRIS
BibTeX
@article{hu2026myf5,
  title = {{Myf5 Progenitors Define the Lineage Identity of Somitic Vascular Smooth Muscle Cells.}},
  author = {Donghua Hu and Kun Chen and Xifeng Chang and Xi Hu and Hongjin Chen and Xingrong Zhai and Xinkai Qu and Lei Fu and Cheng-Chao Ruan and Kailei Shi},
  journal = {International journal of molecular sciences},
  year = {2026},
  month = sep,
  doi = {10.3390/ijms27198594},
  url = {https://europepmc.org/article/MED/42883840},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Myf5 Progenitors Define the Lineage Identity of Somitic Vascular Smooth Muscle Cells.
AU  - Donghua Hu
AU  - Kun Chen
AU  - Xifeng Chang
AU  - Xi Hu
AU  - Hongjin Chen
AU  - Xingrong Zhai
AU  - Xinkai Qu
AU  - Lei Fu
AU  - Cheng-Chao Ruan
AU  - Kailei Shi
PY  - 2026
DA  - 2026/09/25
JO  - International journal of molecular sciences
DO  - 10.3390/ijms27198594
UR  - https://europepmc.org/article/MED/42883840
AB  - Vascular smooth muscle cell (VSMC) heterogeneity drives region-specific aortic pathologies, yet the roles of somite-derived lineages remain unclear. Utilizing Myf5 and MyoD lineage tracing alongside a smooth muscle-specific Myf5 conditional knockout model, we show that Myf5-derived cells selectively populate the thoracic aortic media, whereas the MyoD lineage completely spares large arteries. Early embryonic Myf5 deletion suppressed embryonic VSMC proliferation and downregulated α-SMA, reduced the synthesis of elastic, establishing its necessity in aortic morphogenesis. Upon in vitro ox-LDL challenge and calcification induction, the non-Myf5 lineage primarily drives excessive proliferation and osteogenic transdifferentiation, whereas Myf5 lineage VSMCs exhibit remarkable phenotypic stability and resistance to PDGF-BB-induced dedifferentiation compared to their non-Myf5 counterparts. Collectively, our findings demonstrate a strict lineage divergence between Myf5 and MyoD, suggesting that Myf5 lineage cells play an important role in maintaining aortic integrity, and uncover a lineage-imprinted plasticity that explains regional vascular heterogeneity.
SN  - 1422-0067
ER  -