What is the clinical evidence from this study?

Study design: Observational. Population: Atherosclerosis / Thin-cap fibroatheromata. Primary outcome: Fibroblast activation protein (FAP) expression in type IV-V vs type II-III human aortic atheromata (p=<0.01).

What question did this study set out to answer?

This research aims to investigate the role of fibroblast activation protein (FAP) in collagen degradation within thin-cap fibroatheromata associated with atherosclerosis.

May 15, 2026European Heart JournalOpen Access

Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata

Q: What are the key findings of this study?

Fibroblast activation protein expression was significantly increased in thin-cap versus thick-cap human coronary fibroatheromata (P<0.01) and contributed to type I collagen breakdown.

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

This research aims to investigate the role of fibroblast activation protein (FAP) in collagen degradation within thin-cap fibroatheromata associated with atherosclerosis.

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Key result

Fibroblast activation protein is higher in thin-cap versus thick-cap coronary fibroatheromata, contributing to collagen breakdown.

P<0.01

Why the study?

Collagen degradation renders thin-cap atherosclerotic plaques prone to rupture, but the significance of fibroblast activation protein in thin-cap human fibroatheromata remains unknown.

Population

Human aortic and coronary atheromata tissue specimens and cultured human aortic smooth muscle cells

Comparison

Plaques by lesion type and cap thickness, plus in vitro TNFα stimulation and FAP neutralization

Design

Preclinical translational and in vitro study

Authors

CBChad E. BrokoppUniversity of Zurich RSRoman SchoenauerPsychiatry Baselland PRPeter J. RichardsNovartis (Switzerland)

Discussion

Member takes

Implication

FAP expression may mark vulnerable plaques; leaves open its potential as a therapeutic target for stabilization.

Key Points

This research aims to investigate the role of fibroblast activation protein (FAP) in collagen degradation within thin-cap fibroatheromata associated with atherosclerosis.
Evaluated FAP expression in human aortic atheromata using immunostaining and western blot analyses (n=12 for type IV-V and n=9 for type II-III).
Conducted zymography to assess collagen enzyme activity related to FAP in cultured smooth muscle cells (n=6).
Analyzed correlations between macrophage burden and FAP expression in aortic plaques (n=12).
FAP levels significantly increased in type IV-V lesions compared to type II-III lesions and healthy aortae (P<0.01).
A significant association between macrophage burden and FAP expression was found (R(2)=0.763; P<0.05).
FAP demonstrated collagenase activity by degrading type I collagen in vitro (P<0.01).

Study Design

Type

Observational

Structured PICO

Population

Human aortic atheromata (type IV-V n=12, type II-III n=9), healthy aortae (n=8), human coronary fibroatheromata (thin-cap n=12, thick-cap n=12), and cultured human aortic smooth muscle cells (HASMC).

Intervention

In vitro stimulation with human tumour necrosis factor α (TNFα) and neutralization with an antibody directed against the FAP catalytic domain.

Comparator

Healthy aortae, thick-cap fibroatheromata, and untreated control cells.

Outcome

Fibroblast activation protein (FAP) expression and FAP-mediated type I collagenase activity.surrogate

Main Result

p-value: p=<0.01

FAP is upregulated by macrophage-derived TNFα in human aortic smooth muscle cells and contributes to collagen breakdown in thin-cap fibroatheromata, suggesting a mechanistic role in plaque vulnerability and rupture.

Cite This Study

Brokopp et al. (2011) conducted an observational in Atherosclerosis / Thin-cap fibroatheromata. Fibroblast activation protein expression was significantly increased in thin-cap versus thick-cap human coronary fibroatheromata (P<0.01) and contributed to type I collagen breakdown.

synapsesocial.com/papers/6a078dcbd9ec3070f22dd5ff https://doi.org/10.1093/eurheartj/ehq519

Topics

Coronary artery disease

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Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata

Discussion

Member takes

Implication

Key Points

Study Design

Structured PICO

Main Result

Cite This Study

Topics

Fibroblast activation protein is induced by inflammation and degrades type I collagen in thin-cap fibroatheromata

Discussion

Member takes

Implication

Key Points

Study Design

Structured PICO

Main Result

Cite This Study

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Topics

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