Plaque rupture in humans and mice

Area of Science:

• Cardiovascular Research
• Translational Medicine
• Animal Models

Background:

• Murine atherosclerosis models are widely used but their relevance to human plaque rupture is unclear.
• Current terminology like "vulnerable" or "stable" plaques in mice is often misleading as spontaneous rupture is rare.
• Confusion arises from applying human-specific terms to mouse models lacking proven equivalents.

Purpose of the Study:

• To address the confusion in terminology used for murine atherosclerosis plaque.
• To advocate for a shift towards descriptive, process-focused language in atherosclerosis research.
• To improve the translational relevance of mouse models to human cardiovascular disease.

Main Methods:

• Literature review and conceptual analysis of atherosclerosis terminology.
• Critique of current descriptive terms used in murine models.
• Proposal of an alternative, process-oriented approach to plaque characterization.

Main Results:

• Identified significant ambiguity and potential misinterpretation in current terms like "vulnerable" and "stable" plaques in murine models.
• Highlighted the lack of spontaneous plaque rupture and thrombus formation in mice, questioning direct translation of human terms.
• Demonstrated that specific processes like fibrous cap formation and cell death are well-modeled and objectively measurable.

Conclusions:

• Discourage the use of conclusory terms such as "vulnerable" and "stable" in murine atherosclerosis research.
• Recommend focusing on well-defined, descriptive processes (e.g., fibrous cap formation, protease activation, cell death) for objective modeling.
• Emphasize testing the relevance of mouse model findings against human pathology data for improved translational accuracy.