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Myeloid-Specific Pck1 Deficiency Does Not Alter Aortic Root Atherosclerosis in Mice
Biorxiv : the Preprint Server for Biology
|July 17, 2026
Summary
Phosphoenolpyruvate carboxykinase 1 (Pck1) deficiency in macrophages unexpectedly lowered cholesterol levels in male mice but did not alter atherosclerosis. Pck1 was not confirmed as an atherosclerosis modifier gene.
Area of Science:
- Genetics
- Cardiovascular Biology
- Metabolic Research
Background:
- A quantitative trait locus (QTL), Ath28.1, associated with atherosclerosis was identified on chromosome 2.
- This QTL region contains three protein-coding genes: Zbp1, Pck1, and Pmepa1.
Purpose of the Study:
- To investigate the role of Pck1 in atherosclerosis.
- To determine if Pck1 is an atherosclerosis modifier gene.
Main Methods:
- Macrophage-specific knockout of Pck1 (KO) was created.
- A mouse model overexpressing PCSK9 was used to induce hyperlipidemia and atherosclerosis.
- The effects of Pck1 deficiency were assessed in male and female mice.
Main Results:
- Macrophage Pck1 deficiency reduced body weight, liver weight, and HDL-cholesterol in both sexes.
- Total and non-HDL cholesterol levels decreased only in male KO mice.
- Aortic root and necrotic lesion areas remained unchanged in KO mice.
Conclusions:
- Pck1 deficiency in macrophages did not affect atherosclerosis development.
- Pck1 is not confirmed as an atherosclerosis modifier gene.
