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Inflammation01:38

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Related Experiment Video

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Isolation, Characterization, and Purification of Macrophages from Tissues Affected by Obesity-related Inflammation
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ACKR1hiECs Promote Aortic Dissection Through Adjusting Macrophage Behavior.

Yayu Wang1,2, Xiong Jia1,2, Yifei Zhang1

  • 1Department of Cardiovascular Surgery, The Second Clinical Medical College, Jinan University (Shenzhen People's Hospital), Guangdong, China (Y.W., X.J., Y. Zhang, X.Z., Q.Z.).

Circulation Research
|December 18, 2024
PubMed
Summary

Endothelial cells expressing high ACKR1 promote type A aortic dissection (TAAD) by activating macrophages. Targeting ACKR1 with drugs like amikacin inhibits this pathway, reducing TAAD progression and improving survival.

Keywords:
amikacinanimalsaortic dissectioncell communicationendothelial cellsmacrophages

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Cell Biology

Background:

  • Type A aortic dissection (TAAD) is a severe condition with complex mechanisms.
  • Macrophages play a key role in TAAD pathophysiology, but their precise function is unclear.
  • Endothelial cells (ECs) with elevated atypical chemokine receptor 1 (ACKR1) expression are implicated in TAAD.

Purpose of the Study:

  • To investigate the role of ECs with high ACKR1 expression in TAAD.
  • To elucidate the interaction between ACKR1-expressing ECs and proinflammatory macrophages in TAAD.
  • To identify potential therapeutic targets for TAAD.

Main Methods:

  • Single-cell transcriptomic analysis of human aortic tissues.
  • Clinical and animal studies correlating ACKR1 expression with TAAD severity.
  • In vitro and in vivo gain- and loss-of-function experiments modulating ACKR1 in ECs.
  • Molecular docking and drug screening to identify ACKR1 inhibitors.

Main Results:

  • TAAD tissues showed increased ECs with high ACKR1 and more proinflammatory macrophages.
  • High ACKR1 levels correlated with TAAD severity.
  • ACKR1 knockdown reduced macrophage migration and polarization via the NF-κB/SPP1 pathway, inhibiting TAAD.
  • Amikacin targeted ACKR1, attenuated TAAD progression, and improved survival in mice.

Conclusions:

  • High ACKR1 expression in ECs drives TAAD by promoting macrophage migration and polarization through the ACKR1/NF-κB/SPP1 pathway.
  • Targeting ACKR1, pharmacologically or functionally, suppressed TAAD progression and enhanced survival in preclinical models.
  • ACKR1 represents a promising therapeutic target for TAAD intervention.