What is the clinical evidence from this study?

Study design: Cross-Sectional. Population: Visceral Fat Accumulation (n=78). Primary outcome: Plasma LL37 concentration (ng/mL) (p=<0.001).

What question did this study set out to answer?

This research aims to clarify the connection between visceral fat accumulation, cathelicidin levels, and coronary artery disease.

March 29, 2026Circulation Journal0 citationsOpen Access

Cathelicidin Links Visceral Fat Accumulation and Coronary Artery Disease

Q: What are the key findings of this study?

Plasma cathelicidin (LL37) concentrations were significantly higher in individuals with visceral fat accumulation compared to normal-weight individuals (99.11 vs 58.63 ng/mL).

Q: What question did this study set out to answer?

This research aims to clarify the connection between visceral fat accumulation, cathelicidin levels, and coronary artery disease.

MTMotoki Taniguchi ATA Taruya CKChie Kitahara

Key Result

Plasma cathelicidin (LL37) concentrations were significantly higher in individuals with visceral fat accumulation compared to normal-weight individuals (99.11 vs 58.63 ng/mL).

Key Points

This research aims to clarify the connection between visceral fat accumulation, cathelicidin levels, and coronary artery disease.
Analyzed visceral fat distribution and cathelicidin levels
Investigated the relationship with coronary artery disease
Explored the role of epicardial adipose tissue in inflammation
Found a significant link between elevated cathelicidin levels and visceral fat accumulation
Coronary artery disease severity was associated with increased visceral fat
Implied potential therapeutic role of targeting cathelicidin in CAD management

Study Design

Type

Cross-Sectional (n=78)

Multicenter

Structured PICO

Does visceral fat accumulation correlate with cathelicidin (LL37) levels, and does cathelicidin suppression prevent atherosclerosis?

Population

78 subjects without CAD (stratified into normal-weight, subcutaneous fat, and visceral fat groups), 9 patients undergoing open-heart surgery, and an animal model (WT and Apoe-/- mice)

Intervention

CRAMP siRNA (in animal model)

Comparator

Scrambled siRNA or vehicle (in animal model)

Outcome

Plasma LL37 concentrations across obesity groups, LL37 expression in epicardial adipose tissue (EAT), and atherosclerotic lesion area in micesurrogate

Plasma LL37 concentrations correlate with visceral fat accumulation and epicardial adipose tissue, and suppressing cathelicidin reduces atherosclerosis in mice, suggesting LL37 as a potential biomarker and therapeutic target for obesity-related CAD.

Main Result

Absolute Event Rate: 99.11% vs 58.63%

p-value: p=<0.001

Limitations

CRAMP knockdown was assessed at a single time point, leaving temporal dynamics and long-term effects unclear.
Japanese single-center study with a relatively small sample size.
EAT samples were surgically obtained, meaning sampling errors cannot be excluded.
Cross-sectional design precludes inferring causal relationships between LL37 expression and CAD or obesity-related phenotypes.
Tissue-based analyses were limited by small sample size and lacked direct functional validation.

Abstract

Background: Visceral fat (VF), particularly epicardial adipose tissue (EAT), plays a crucial role in the development of coronary artery disease (CAD). Cathelicidin (LL37) is an antimicrobial peptide involved in innate immunity and has been implicated in inflammatory processes. However, the relationship between VF accumulation, cathelicidin, and atherosclerosis remains unclear.

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