Authors
Shwethali Wani, Michael Kitching, Sobhan Aboulhassanzadeh, Teodora-Simona Lungu, Isil Kilicgun, Karsyn Ulibarri, Weimin Liu, Achilleas Floudas, Eileen M Redmond, Paul A Cahill
Published in
bioRxiv : the preprint server for biology. Jul 24, 2026. Epub Jul 24, 2026.
Abstract
The cellular origin of smooth muscle cell (SMC)-derived populations in vascular lesions remains unresolved. Here we show, using single-cell transcriptomic analyses spanning carotid ligation injury, Myh11-CreERT²-traced aortic homeostasis, and LDLR- and ApoE-deficient atherosclerosis, that a rare progenitor-like "Primed" SMC compartment pre-exists at baseline in all models and in the healthy human aorta. Relative to contractile SMCs, Primed SMCs attenuate sarcomeric and contractile programmes while inducing matricellular, progenitor-niche and chondrogenic-poised developmental programmes, resolving into conserved niche/progenitor ( Cd34, Fst, Tnfrsf11b ) and matricellular ( Vcam1, Thbs1, Timp1 ) cores overlaid by vessel-specific signatures, on a retained SMC identity. Multiple orthogonal computational lineage-inference approaches indicate that this compartment expands predominantly through autonomous self-renewal and is the dominant inferred source of cycling and lesion fibrochondrocyte populations, while contractile SMCs are consistently depleted as a feeder source. These findings reframe lesional SMC cellularity as expansion of a pre-existing Primed compartment rather than widespread phenotypic switching of contractile SMCs.
PMID:
42539223
Bibliographic data and abstract were imported from PubMed on 01 Aug 2026.
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