Abdominal Aortic Aneurysm and Liver Fibrosis: Clinical Evidence and Molecular Pathomechanisms

TL;DR

This review explores how liver fibrosis may be linked to abdominal aortic aneurysms, focusing on shared risk factors and potential molecular mechanisms.

Contribution

The paper provides a novel synthesis of clinical and molecular evidence linking liver fibrosis with abdominal aortic aneurysm development.

Findings

Liver fibrosis and metabolic dysfunction-associated steatotic liver disease may share inflammatory pathways with abdominal aortic aneurysms.

Systemic inflammation, oxidative stress, and extracellular matrix remodeling are potential shared mechanisms between liver fibrosis and AAA.

Type 2 diabetes, female sex, and certain ethnicities may be protective against AAA, but further research is needed to confirm this.

Abstract

To stimulate further research, this review summarizes studies linking liver fibrosis with the risk of abdominal aortic aneurysms (AAA). AAA is defined as a permanently weakened and dilated abdominal aorta, which develops due to inflammation of the tunica media, activation of the renin–angiotensin–aldosterone system, immune system activation, and coagulation disorders. Typically asymptomatic, AAA is often incidentally detected through imaging done for abdominal symptoms or as part of screening programs. AAA follows a variable course and has a mortality rate strongly dependent on age and sex. Risk factors for AAA include age, male sex, ethnicity, family history of AAA, lifestyle habits, arterial hypertension, dyslipidemia, and comorbid atherosclerotic cardiovascular disease. Conversely, individuals with type 2 diabetes, female sex, and certain ethnicities are at a reduced risk of AAA. Liver fibrosis, resulting from chronic liver diseases owing to varying etiologies, is increasingly recognized as a potential contributor to AAA development. Evidence increasingly indicates that metabolic dysfunction-associated steatotic liver disease (MASLD) and other chronic liver conditions may intensify inflammatory pathways shared with AAA, thereby potentially exacerbating AAA progression. This review specifically examines the epidemiology and risk factors associated with the link between AAA and liver fibrosis. It also highlights potential pathomechanisms, including systemic inflammation, oxidative stress, and extracellular matrix remodeling, which may contribute to both conditions. Although these findings underscore significant overlaps in risk profiles, additional research is needed to clarify whether type 2 diabetes, female sex, and certain ethnicities truly confer protection against AAA or if this association is influenced by other confounding variables. Ultimately, addressing these open questions will help guide targeted therapeutic interventions and the identification of novel biomarkers to predict disease progression.

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