What question did this study set out to answer?

To determine whether the chemokine fractalkine and its receptor CX3CR1 are critically required for the development of atherosclerotic lesions.

February 1, 2003Journal of Clinical InvestigationOpen Access

Decreased atherosclerosis in CX3CR1–/– mice reveals a role for fractalkine in atherogenesis

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To determine whether the chemokine fractalkine and its receptor CX3CR1 are critically required for the development of atherosclerotic lesions.
Generated CX3CR1-knockout mice and crossed them into an apolipoprotein E-deficient (apoE-/-) background.
Fed the mice a high-fat diet to stimulate atherogenesis and evaluated fractalkine expression, macrophage recruitment, and plaque development.
Fractalkine was robustly expressed within lesional smooth muscle cells of apoE-/- mice, but was not detected in macrophages.
CX3CR1-deficient mice exhibited a significant reduction in macrophage recruitment to the vessel wall alongside decreased atherosclerotic lesion formation.

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Implication

Experimental study demonstrates reduced macrophage recruitment and lesion formation in CX3CR1-deficient mice, indicating fractalkine drives atherogenesis.

Cite This Study

Lesnik et al. (2003) studied this question.

synapsesocial.com/papers/6a700e7d26770c2b8de04c27 https://doi.org/10.1172/jci15555

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Implication

Experimental study demonstrates reduced macrophage recruitment and lesion formation in CX3CR1-deficient mice, indicating fractalkine drives atherogenesis.

Decreased atherosclerosis in CX3CR1–/– mice reveals a role for fractalkine in atherogenesis

Key Points

Discussion

Implication

Cite This Study

Decreased atherosclerosis in CX3CR1–/– mice reveals a role for fractalkine in atherogenesis

Key Points

Discussion

Implication

Cite This Study