Lab-grown blood vessels pinpoint which cell type drives rapid aging damage
Shores KL, Gao XD, Liu DR, Truskey GA
Tissue Engineering
This study is about human biomedical research, not plants, so there's no direct connection to your garden or the trees in your park.
Researchers built a tiny artificial blood vessel in the lab using three types of human cells layered together, mimicking real arteries. They used it to study a rare disease that causes extremely fast aging, and discovered that one of the three cell types, the structural fibroblasts, was responsible for much of the tissue damage seen in the disease. Fixing the disease-causing gene with a gene-editing tool brought the vessel back closer to healthy.
Key Findings
A trilayer tissue-engineered blood vessel (TEBV) combining smooth muscle cells, endothelial cells, and fibroblasts was used to model Hutchinson-Gilford progeria syndrome (HGPS)
HGPS fibroblasts specifically drove extracellular matrix dysregulation and fibrotic signaling, while smooth muscle cells drove collagen buildup and endothelial cells drove inflammation
Base editing to correct the HGPS mutation restored many disease features in the engineered vessels to near-healthy levels
chevron_right Technical Summary
Scientists built a lab-grown three-layer blood vessel using human cells to study Hutchinson-Gilford progeria, a rare rapid-aging disease, and found that fibroblasts (the vessel's structural cells) play an outsized role in driving the disease's hallmark artery damage.
Abstract Preview
Original paper
Human trilayer engineered blood vessel reveals influence of fibroblasts on disease progression in model of Hutchinson-Gilford progeria.
In vitro models of vascular disease have focused primarily on the pathophysiology of smooth muscle cell (SMC) or endothelial cell (EC). Adventitial fibroblasts can contribute to disease progression...
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