What question did this study set out to answer?

To examine how perivascular adipose tissue and obesity-related inflammatory mediators drive the pathogenesis and progression of abdominal aortic aneurysms.

August 21, 2026European Heart JournalOpen Access

Linking obesity with abdominal aortic aneurysm development

Q: What is the clinical evidence from this study?

Study design: Editorial. Population: Abdominal aortic aneurysm. Intervention: Deletion of NCC and/or IL18r. Primary outcome: Abdominal aortic aneurysm progression.

Q: What does this research mean for the field?

Single or combined deletion of the interleukin-18 receptors IL18r and NCC attenuates abdominal aortic aneurysm progression in murine models. Novelty: ClaimNovelty.NOVEL_FINDING. Consensus alignment: ConsensusAlignment.NEUTRAL.

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Key result

Combined and single deletion of NCC and/or IL18r limited murine abdominal aortic aneurysm progression.

Why the study?

Does deletion of NCC and/or IL18r prevent abdominal aortic aneurysm progression in murine models?

Key Points

To examine how perivascular adipose tissue and obesity-related inflammatory mediators drive the pathogenesis and progression of abdominal aortic aneurysms.
Reviewed preclinical experiments using murine models of angiotensin II-induced abdominal aortic aneurysm with perivascular fat transplants from obese, lean, and leptin-deficient mice.
Evaluated the impact of single and combined genetic deletions of interleukin-18 receptors, specifically IL18r and the Na–Cl co-transporter (NCC).
Assessed clinical relevance using published human histological and epidemiological datasets on aortic dilation and surgical outcomes.
Perivascular adipose tissue from diet-induced obese or lean mice aggravated angiotensin II-induced aneurysm development, whereas tissue from leptin-deficient ob/ob mice did not.
Single or combined knockout of IL18r and NCC limited aneurysm expansion in mice, though single knockouts displayed higher residual macrophage infiltration, matrix metalloproteinase activity, and smooth muscle cell loss than double knockouts.
Untreated aneurysm rupture carries a mortality rate of 97.2%, which drops to 24.7% with endovascular repair and 37.3% with open surgical repair.

Structured PICO

Does deletion of NCC and/or IL18r prevent abdominal aortic aneurysm progression in murine models?

Population

Murine models of angiotensin II-induced abdominal aortic aneurysm

Intervention

Deletion of NCC and/or IL18r

Outcome

Abdominal aortic aneurysm progression

Limitations

Requires additional experiments in pre-clinical large animal models before clinical studies can be performed
Requires validation in large animal models before clinical trials

Implication

Targeting IL-18 and its receptors represents a potential novel therapeutic strategy to limit abdominal aortic aneurysm progression.

Abstract

Discussion

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Published by European Heart Journal · CC BY-NC

Cite This Study

Eckstein et al. (2019) conducted an editorial in Abdominal aortic aneurysm. Deletion of NCC and/or IL18r was evaluated on Abdominal aortic aneurysm progression. Combined and single deletion of NCC and/or IL18r limited murine abdominal aortic aneurysm progression.

synapsesocial.com/papers/6a886c670ed92560a2186384 https://doi.org/10.1093/eurheartj/ehz882

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Implication

Targeting IL-18 and its receptors represents a potential novel therapeutic strategy to limit abdominal aortic aneurysm progression.

Linking obesity with abdominal aortic aneurysm development

Key Points

Structured PICO

Limitations

Implication

Abstract

Discussion

Figures from the paper

Cite This Study

Linking obesity with abdominal aortic aneurysm development

Key Points

Structured PICO

Limitations

Implication

Abstract

Discussion

Figures from the paper

Cite This Study

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