Level D· Scientific groundwork from lab and animal studiesNarrative ReviewEurope PMCOpen access

Emerging Mechanisms of Abdominal Aortic Aneurysm

Zhu B., Chen YE., Guo Y.

Narrative Review on Chronic Inflammation, Immune Modulation, published in Curr Atheroscler Rep (2026) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Narrative Review
Journal
Curr Atheroscler Rep (2026)
Reported sample size
—
Source database
Europe PMC
PMID
41615587
PMCID
PMC12858482
DOI
10.1007/s11883-026-01392-5

Abstract (original English)

PURPOSE OF REVIEW: Abdominal aortic aneurysm (AAA) is a progressive and often fatal vascular disease for which effective pharmacological therapies are lacking. This review synthesizes recent mechanistic advances in AAA pathogenesis and evaluates their translational significance for therapeutic development. RECENT FINDINGS: Single-cell and spatial transcriptomic findings have delineated marked cellular heterogeneity within aneurysmal tissue, revealing dynamic interactions among vascular and immune cell populations. Vascular smooth muscle cell phenotypic modulation and programmed cell death compromise aortic wall integrity, while endothelial dysfunction promotes leukocyte recruitment and mediates early vascular responses. Infiltrating macrophages, neutrophils, and adaptive immune cells orchestrate chronic inflammation and extracellular matrix degeneration, whereas eosinophils and regulatory T cells exert context-dependent protective effects. Local factors, including intraluminal thrombus and perivascular adipose tissue, as well as systemic modulators such as dyslipidemia, gut microbiota, and sex hormones, further shape disease initiation and progression. These mechanistic insights have identified novel therapeutic targets, including inhibitors of regulated cell death, immunomodulatory agents, lipid-lowering interventions, and microbiome-directed strategies, and potential biomarke

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is a narrative review: it collects no new patient data and does not systematically appraise evidence quality.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Muscle, Smooth, VascularAnimalsHumansAortic Aneurysm, AbdominalDisease ProgressionInflammation

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