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0This article identifies a specific population of smooth muscle-derived transient progenitor cells (STPCs) that emerge following vascular injury to drive pathological remodeling. Marked by the expression of CD34, these cells originate from mature smooth muscle cells through a process of temporary dedifferentiation, gaining high proliferative capacity and the ability to differentiate into multiple lineages. Researchers utilized dual-recombinase lineage tracing to prove that STPCs are the primary source of neointimal hyperplasia, which is a central feature of cardiovascular diseases like atherosclerosis. The study further establishes that the protein DCLK1 acts as a vital molecular regulator for the transition of smooth muscle cells into this progenitor state. Ultimately, the findings suggest that genetically ablating STPCs or inhibiting DCLK1 can significantly reduce arterial thickening, identifying them as promising therapeutic targets.
References:
Lu Y, Ni H, Shen J, et al. Smooth muscle cells transiently acquire a CD34+ progenitor state upon injury to drive pathological vascular remodeling[J]. Cell Stem Cell, 2026.
