Smooth muscle cells transiently acquire a CD34<sup>+</sup> progenitor state upon injury to drive pathological vascular remodeling.
basic_science · Level V
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- Record sourced from PubMed, PMID 42190659.
- Also identified by DOI 10.1016/j.stem.2026.04.023.
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Abstract
Neointimal hyperplasia, a key pathological feature of many cardiovascular diseases, is driven by vascular smooth muscle cells (SMCs), yet the role of specific SMC subtypes remains unclear. This study identifies a smooth muscle-derived transient progenitor cell (STPC) population, marked by CD34 expression, which emerges after artery injury. These STPCs exhibit high proliferative capacity and generate the majority of neointimal SMCs. Genetic ablation of STPCs significantly reduces neointimal SMC accumulation and attenuates hyperplasia. Mechanistically, SMC-specific knockdown of DCLK1 markedly suppresses STPC generation and mitigates pathological remodeling. These findings establish STPCs as a critical progenitor population responsible for neointimal hyperplasia, identifying them as a novel therapeutic target for vascular diseases.