Adhesion molecule with Ig-like domain 1 regulates stability of carotid plaque via TGFβ/Smad signaling pathway by

Xintao Hu1, Xiaoqing Li1, Jichong Chen1

  • 1Department of Vascular Surgery, The Fifth Affiliated Hospital of Zhengzhou University, No. 3 Kangfuqian Street, Erqi District, Zhengzhou 450052, Henan, China.

Cellular Signalling
|February 14, 2026
PubMed

Insights

AMIGO1 protein stabilizes carotid atherosclerosis plaques by enhancing endothelial cell adhesion and reducing inflammation. It interacts with TGFRII, activating the TGFβ pathway to protect against stroke and related events.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Atherosclerosis Research

Background:

  • Carotid atherosclerosis is a major risk factor for cardiovascular and cerebrovascular diseases.
  • Maintaining plaque stability is crucial for preventing stroke and transient ischemic attack (TIA).
  • Mechanisms governing carotid plaque stability remain incompletely understood.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying carotid plaque stability.
  • To identify novel therapeutic targets for carotid atherosclerosis (CAS).

Main Methods:

  • RNA-sequencing of stable and unstable carotid plaques.
  • Functional assays (cell adhesion, cytokine detection).
  • Co-immunoprecipitation (Co-IP) and in vivo mouse models (ApoE-/-).

Main Results:

  • 594 differentially expressed genes identified; AMIGO1 significantly upregulated in stable plaques.
  • AMIGO1 promotes endothelial cell adhesion and downregulates inflammatory cytokines (IL-6, IL-1β, TNF-α).
  • AMIGO1 interacts with TGFRII, stabilizing it and activating the TGFβ/SMAD pathway, thereby stabilizing carotid plaques in vivo.

Conclusions:

  • AMIGO1 is a key regulator of carotid plaque stability.
  • AMIGO1 exerts protective effects by enhancing endothelial function and reducing inflammation via the TGFβ/SMAD pathway.
  • AMIGO1 represents a potential therapeutic target for carotid atherosclerosis.

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