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Smooth muscle contraction is a complex process vital for various bodily functions, from maintaining blood vessel tension to facilitating the movement of food through the digestive tract. Unlike striated muscles, smooth muscle contraction begins more slowly and lasts longer.
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Related Experiment Video

Updated: May 10, 2025

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CCDC80 Protects against Aortic Dissection and Rupture by Maintaining the Contractile Smooth Muscle Cell Phenotype.

Qingqing Xiao1,2, Yi Li1, Bin Cai3

  • 1Department of Cardiology, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200030, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|April 25, 2025
PubMed
Summary

Coiled-coil domain-containing protein 80 (CCDC80) deficiency exacerbates aortic dissection (AD) by activating the JAK2/STAT3 pathway, impacting vascular smooth muscle cell function. CCDC80 is a potential therapeutic target for AD.

Keywords:
CCDC80JAK2/STAT3 signaling pathwayVSMC phenotype switchingaortic dissectionvascular remodeling

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Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Vascular Biology

Background:

  • Aortic dissection (AD) is a critical condition involving adverse vascular remodeling.
  • Coiled-coil domain-containing protein 80 (CCDC80) is implicated in cardiovascular remodeling.
  • The specific role of CCDC80 in AD pathogenesis requires elucidation.

Purpose of the Study:

  • To investigate the role of CCDC80 in the development and progression of aortic dissection.
  • To elucidate the molecular mechanisms by which CCDC80 influences vascular smooth muscle cell (VSMC) behavior in AD.

Main Methods:

  • Analysis of CCDC80 expression in human and mouse AD models.
  • Generation and assessment of CCDC80 knockout and VSMC-specific CCDC80 knockout mouse models subjected to hypertension-inducing stimuli (Ang II, BAPN).
  • Investigation of the JAK2/STAT3 signaling pathway and its interaction with CCDC80 in VSMCs.

Main Results:

  • CCDC80 is significantly downregulated in VSMCs from human and mouse AD.
  • CCDC80 deficiency in mice leads to increased frequency and severity of AD, characterized by elastin fragmentation and collagen deposition.
  • CCDC80 deficiency activates the JAK2/STAT3 pathway, promoting VSMC dedifferentiation, proliferation, migration, and matrix metalloproteinase production.

Conclusions:

  • CCDC80 deficiency exacerbates AD progression by activating the JAK2/STAT3 pathway, which dysregulates VSMC phenotype and function.
  • Targeting CCDC80 may offer a novel therapeutic strategy for preventing and treating aortic dissection.