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Related Experiment Video

Updated: Dec 25, 2025

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
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Smooth Muscle Cell Reprogramming in Aortic Aneurysms.

Pei-Yu Chen1, Lingfeng Qin2, Guangxin Li3

  • 1Yale Cardiovascular Research Center, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA.

Cell Stem Cell
|April 4, 2020
PubMed
Summary
This summary is machine-generated.

Aortic aneurysms involve smooth muscle cell reprogramming into a stem cell-like state. Disrupting TGF-β signaling in these cells triggers aneurysm development, mimicking human disease features.

Keywords:
TGF-betaaneurysmaortaartificial intelligenceatherosclerosiscell fatecell reprogrammingmesenchymal stem cellscRNA-seqsmooth muscle cells

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Area of Science:

  • Cardiovascular Biology
  • Cellular Reprogramming
  • Atherosclerosis Research

Background:

  • Aortic aneurysm etiology is unclear, linked to atherosclerosis, hypercholesterolemia, and TGF-β signaling.
  • Smooth muscle cells (SMCs) play a critical role in aortic wall integrity.

Purpose of the Study:

  • Investigate the interplay of atherosclerosis, hypercholesterolemia, and TGF-β signaling in aortic aneurysm development.
  • Identify the role of SMC reprogramming in aneurysm pathogenesis.

Main Methods:

  • Utilized Apoe-/- mice on a hypercholesterolemic diet.
  • Performed SMC-specific ablation of transforming growth factor β (TGF-β) signaling.
  • Analyzed aortic tissue for cellular changes, calcification, and inflammation.

Main Results:

  • SMC-specific TGF-β signaling disruption induced aortic aneurysms with human disease features.
  • Aneurysms were associated with SMCs transdifferentiating into a mesenchymal stem cell (MSC)-like state.
  • This reprogramming generated various cell types (osteoblasts, chondrocytes, adipocytes, macrophages), leading to medial SMC loss and increased non-SMC mass.

Conclusions:

  • SMC reprogramming into an MSC-like state is a key mechanism in aortic aneurysm development.
  • Aberrant TGF-β signaling in SMCs drives this reprogramming, contributing to aortic dilation, calcification, and inflammation.
  • Targeting SMC reprogramming may offer novel therapeutic strategies for aortic aneurysms.