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<p>Co-presentation of carotid plaque (CPL) and abdominal aortic aneurysm (AAA) is frequent and synergy in the development proposed. Inflammatory mediators affect this growth but their interplay in inducing single or multiple vascular damage scarcely explored. Healthy people and characterized male patients undergoing aneurysmectomy or endarterectomy with significant/not significant CPL and large AAA or no/small AAA were allocated to groups. CPL distribution along the carotid branches differed in patients without vs. with large AAA. ELISA and 15plex Luminex assays in serum and lesioned arteries revealed intergroup differences in the content of P2X7, GM-CSF, CXCL1, IL-1β, IL-10, IL-12p70, CCL 3, TNFα, and RT-qPCR in the expression of P2X7-targeting microRNA, namely miR-150. These data identified group-distinctive inflammatory fingerprints, stratifying patients. In silico analysis of fingerprints showed GO processes common/exclusive to groups, supporting mechanistic difference associated to lesion presentation. In vitro aortic endothelial cells respond to serum from patients with both AAA and CPL but not with only CPL, increasing P2X7, IL1B and CXCL1 genes and P2X7 isoforms, hinting to a relation between serum fingerprints and artery type. Fingerprinting may represent a stratifying tool for patients with CPL and AAA; P2X7, GM-CSF, IL-1β and CXCL1 emerge as potential candidates for personalized monitoring and therapy.</p>

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P2X7 and inflammatory fingerprinting of patients with carotid atherosclerosis and the risk of abdominal aortic aneurysm

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月7日

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  • Maria Lombardi,
  • Lucia Spartano,
  • Vincenzo Ardita,
  • Ferdinando B. A. Valente,
  • Nicola Galati,
  • Renata Castellano,
  • Roberto Chiesa,
  • Domenico Baccellieri,
  • Chiara Foglieni

摘要

Co-presentation of carotid plaque (CPL) and abdominal aortic aneurysm (AAA) is frequent and synergy in the development proposed. Inflammatory mediators affect this growth but their interplay in inducing single or multiple vascular damage scarcely explored. Healthy people and characterized male patients undergoing aneurysmectomy or endarterectomy with significant/not significant CPL and large AAA or no/small AAA were allocated to groups. CPL distribution along the carotid branches differed in patients without vs. with large AAA. ELISA and 15plex Luminex assays in serum and lesioned arteries revealed intergroup differences in the content of P2X7, GM-CSF, CXCL1, IL-1β, IL-10, IL-12p70, CCL 3, TNFα, and RT-qPCR in the expression of P2X7-targeting microRNA, namely miR-150. These data identified group-distinctive inflammatory fingerprints, stratifying patients. In silico analysis of fingerprints showed GO processes common/exclusive to groups, supporting mechanistic difference associated to lesion presentation. In vitro aortic endothelial cells respond to serum from patients with both AAA and CPL but not with only CPL, increasing P2X7, IL1B and CXCL1 genes and P2X7 isoforms, hinting to a relation between serum fingerprints and artery type. Fingerprinting may represent a stratifying tool for patients with CPL and AAA; P2X7, GM-CSF, IL-1β and CXCL1 emerge as potential candidates for personalized monitoring and therapy.