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Overview of Cell-Matrix Interactions01:24

Overview of Cell-Matrix Interactions

The extracellular matrix or ECM holds cells together to form a tissue and allows the cells within the tissue to communicate. ECM comprises proteins such as fibronectin, collagen, laminin, etc. The most abundant protein in this space is collagen. Collagen fibers are interwoven with carbohydrate-containing protein molecules called proteoglycans. ECM allows cell migration and provides a structural scaffold at cell adhesion that anchors the cell when the extracellular matrix proteins interact with...

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Updated: May 12, 2026

Three-Dimensional Imaging of Aortic Tissues in Atherosclerosis
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Published on: October 25, 2024

Integrated Single-Cell and Spatial Analysis Reveals a Metabolic-Immune Axis Driving Aortic Dissection.

Jing Tao1,2, Huanjie Yang3,4, Jiahui Yong1,2

  • 1Department of Cardiology, People's Hospital of Xinjiang Uygur Autonomous Region, Urumqi, Xinjiang, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|May 10, 2026
PubMed
Summary
This summary is machine-generated.

Aortic dissection (AD) risk increases with fibroblast loss and vascular smooth muscle cell (vSMC) reprogramming. Targeting ENO1 may reduce inflammation and slow AD progression, offering potential therapeutic strategies.

Keywords:
MIFaortic dissectionenolase 1fibroblastmacrophagesingle‐cell RNA sequencingspatial transcriptomics

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Area of Science:

  • Cardiovascular Biology
  • Translational Medicine
  • Genomics

Background:

  • Mechanisms of aortic dissection (AD) are not fully understood due to limited patient cohorts.
  • Existing single-cell studies provide some insight into diseased aortas.

Purpose of the Study:

  • To create a comprehensive cellular-molecular atlas of the thoracic aorta.
  • To elucidate the cellular and molecular mechanisms driving aortic dissection.

Main Methods:

  • Integration of single-cell and spatial transcriptomic data from 110 thoracic aortic samples.
  • Analysis of samples from control, aneurysm, and dissection groups (80 individuals).
  • Identification of cell subsets and molecular pathways involved in AD pathogenesis.

Main Results:

  • A novel elastin-rich fibroblast subset (Fibro_C1_FBN1+) declines with age and is depleted in AD, increasing aortic vulnerability.
  • Vascular smooth muscle cells (vSMCs) reprogram under hypoxia (ENO1-driven), lose contractility, and promote inflammation and extracellular matrix degradation.
  • ENO1 knockdown in vitro and in vivo reduced vSMC switching, macrophage inflammation, and slowed AD progression.

Conclusions:

  • A stromal-immune axis involving fibroblasts and vSMCs plays a critical role in AD.
  • Fibroblast depletion and vSMC reprogramming contribute to aortic wall vulnerability and dissection risk.
  • Targeting ENO1 and the identified stromal-immune interactions presents potential therapeutic avenues for AD.