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Related Concept Videos

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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The inflammatory response is the body's defense against infection, injury, or irritation from bacteria, trauma, toxins, or heat. Inflammation helps locate and destroy pathogens and remove damaged tissue elements to heal the body. During this initial phase, fluid, blood products, and nutrients migrate to the injured area, resulting in redness, heat, swelling, ache, and loss of function. Moreover, signs of systemic inflammation include fever, increased WBC count, malaise, anorexia, nausea,...
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Related Experiment Video

Updated: Jan 15, 2026

Murine Model of Thoracic Aortic Dissection Induced by Oral β-Aminopropionitrile and Subcutaneous Angiotensin II Infusion
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Complement C3/C3a-CCL9 feedback loop orchestrates inflammatory crosstalk to accelerate aortic dissection.

Xiaodan Zhong1, Yu Li1, Yang Xie2

  • 1Department of Cardiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030 Hubei, China; Hubei Provincial Engineering Research Center of Vascular Interventional Therapy, Wuhan 430030 Hubei, China.

Biochemical Pharmacology
|October 15, 2025
PubMed
Summary

A novel C3/C3a-CCL9 inflammatory feedback loop drives aortic dissection (AD) progression. Blocking C3 activation with CP40KK reduced inflammation, preserved aortic integrity, and improved survival in AD mice.

Keywords:
Aortic dissectionCCL9Complement C3aMacrophage recruitmentVascular smooth muscle cells (VSMCs)

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Area of Science:

  • Vascular Biology
  • Immunology
  • Complement System

Background:

  • Aortic dissection (AD) involves inflammation and immune cell infiltration.
  • The precise roles of complement component 3 (C3) and C3a in AD pathogenesis are not fully understood.

Purpose of the Study:

  • To investigate the role of C3/C3a and identify downstream effectors in AD.
  • To explore C3a-mediated signaling in vascular smooth muscle cells (VSMCs) and its impact on macrophage recruitment.
  • To evaluate the therapeutic potential of C3 inhibition in AD.

Main Methods:

  • Quantification of C3/C3a in human and mouse AD samples.
  • Macrophage depletion studies to identify C3a source.
  • Transcriptomic profiling of C3a-stimulated VSMCs.
  • In vivo studies using a mouse model of AD treated with a C3 inhibitor (CP40KK).

Main Results:

  • Elevated C3a, but not C3, was found in AD patients and mice, originating predominantly from macrophages.
  • C3a stimulation induced VSMC phenotypic switching and CCL9 secretion, recruiting macrophages via C3aR and CCR1.
  • CCL9 amplified the inflammatory response by promoting macrophage recruitment and C3 synthesis, creating a positive feedback loop.
  • CP40KK treatment attenuated C3a and CCL9, reduced macrophage infiltration, preserved aortic integrity, and improved survival in AD mice.

Conclusions:

  • A C3/C3a-CCL9 feedback loop is a critical driver of AD progression.
  • VSMCs act as active regulators of vascular inflammation in AD.
  • C3a and CCL9 are potential therapeutic targets for AD intervention.