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The apolipoprotein e knockout mouse: a model documenting accelerated atherogenesis in uremia.
Moriz Buzello1, Johannes Törnig, Jörg Faulhaber
1Department of Pathology, University of Erlangen-Nürnberg, Erlangen, Germany.
Journal of the American Society of Nephrology : JASN
|January 23, 2003
Summary
Apolipoprotein E knockout (Apoe-/-) mice with mild renal dysfunction showed significantly increased atherosclerosis. This model is valuable for studying renal dysfunction
Area of Science:
- Cardiovascular Science
- Nephrology
- Animal Models
Background:
- Rodents lack spontaneous atherosclerosis, limiting study of uremia's cardiovascular effects.
- Apolipoprotein E knockout (Apoe-/-) mice exhibit lipid abnormalities and atherosclerosis, making them a potential model.
Purpose of the Study:
- To evaluate the utility of apolipoprotein E knockout (Apoe-/-) mice in modeling renal dysfunction's impact on cardiovascular risk.
- To assess the effect of induced renal dysfunction on atherosclerosis development in Apoe-/- mice.
Main Methods:
- Ten-week-old Apoe-/- mice underwent subtotal nephrectomy (SNX), uninephrectomy (UNX), or sham operation.
- Control C57/BL6 mice underwent similar procedures.
- Blood pressure, serum lipid levels, and aortic/intramyocardial artery morphology were analyzed after 12 weeks.
Main Results:
- Apoe-/- mice exhibited higher baseline cholesterol and triglycerides.
- Renal dysfunction (UNX and SNX) significantly increased atherosclerotic plaque size and progression in Apoe-/- mice compared to controls.
- Plaques were foam cell-rich with minimal inflammatory cell infiltration.
Conclusions:
- Even mild renal dysfunction dramatically exacerbates atherosclerosis in Apoe-/- mice.
- The Apoe-/- mouse model is suitable for studying the cardiovascular risks associated with renal dysfunction.
- Induced renal dysfunction promotes aggressive, early-stage atherosclerotic plaque formation.