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Updated: Jun 7, 2025
Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
Published on: September 26, 2018
ECH 1 attenuates atherosclerosis by reducing macrophage infiltration and improving plaque stability through CD36
Caijun Rao1, Haojie Qin2, Zhipeng Du3
1Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Insights
Enoyl coenzyme A hydratase 1 (ECH1) protein levels are elevated in coronary artery disease patients. ECH1 reduces atherosclerotic plaque severity by promoting CD36 degradation, offering a potential therapeutic target.
Area of Science:
- Cardiovascular Biology
- Metabolic Disease Research
- Protein Biochemistry
Background:
- Enoyl coenzyme A hydratase 1 (ECH1) is a secreted protein linked to metabolic disorders.
- The role of ECH1 in atherosclerosis pathogenesis is not well understood.
- Elevated ECH1 levels are observed in coronary artery disease (CAD) patients.
Purpose of the Study:
- To investigate the role of ECH1 in the development of atherosclerosis.
- To explore the potential of ECH1 as a therapeutic target for atherosclerosis.
Main Methods:
- Serum ECH1 levels were measured in CAD patients and apolipoprotein E knockout (ApoE-/-) mice.
- Recombinant ECH1 was administered to ApoE-/- mice to assess its in vivo effects on atherosclerotic plaques.
- In vitro studies using peritoneal macrophages examined the effects of ECH1 on oxidized low-density lipoprotein (oxLDL) uptake and migration.
- Mechanistic studies investigated the impact of ECH1 on scavenger receptor CD36 expression and degradation.
Main Results:
- Higher serum ECH1 levels were found in CAD patients and ApoE-/- mice on a western diet.
- In vivo administration of ECH1 reduced aortic lesions, inflammation, and macrophage infiltration in ApoE-/- mice.
- In vitro, ECH1 decreased oxLDL uptake and enhanced macrophage migration.
- ECH1 promoted lysosome-dependent degradation of scavenger receptor CD36 in macrophages.
Conclusions:
- ECH1 attenuates atherosclerotic plaque severity and improves plaque stability by reducing macrophage infiltration.
- ECH1 exerts its protective effects via enhancing lysosome-dependent CD36 degradation.
- ECH1 represents a promising therapeutic target for atherosclerosis prevention and treatment.
Abstract:
Enoyl coenzyme A hydratase 1 (ECH1) is a secreted protein implicated in numerous metabolic disorders, yet its role in the pathogenesis of atherosclerosis remains unclear. In this study, we found higher serum ECH1 levels in coronary artery disease (CAD) patients and apolipoprotein E (ApoE)-/- mice on a western diet for 12 weeks. In vivo, aorta and aortic sinus histological staining revealed that intraperitoneal injection of recombinant ECH1 reduced aortic lesions, inflammation, and macrophage infiltration in ApoE-/- mice. In vitro, incubating peritoneal macrophages with recombinant ECH1 protein reduced oxidized low-density lipoprotein uptake and increased macrophage migration. Mechanically, we observed that recombinant ECH1 incubation led to a reduction in the protein levels of scavenger receptor cluster of differentiation 36 (CD36) in primary macrophages through the promotion of CD36 protein degradation. Additionally, we found that chloroquine (CQ), a lysosomal inhibitor, mitigated this pro-degradation effect. Taken together, our findings provide unique evidence that ECH1 can attenuate the severity of atherosclerotic plaques, especially improving the stability of plaques, by decreasing macrophage infiltration. ECH1 demonstrates its protective effect by enhancing the lysosome-dependent degradation of CD36, suggesting its potential as a viable target for the prevention and treatment of atherosclerosis.
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