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Updated: Dec 27, 2025

In Vitro Analysis of E3 Ubiquitin Ligase Function
Published on: May 14, 2021
The Role of Ubiquitin E3 Ligase in Atherosclerosis
Zhi-Xiang Zhou1, Zhong Ren1, Bin-Jie Yan1
1Institute of Cardiovascular Disease, Key Laboratory for Arteriosclerosis of Hunan Province, Hengyang Medical College, University of South China, Hengyang City, Hunan Province 421001, China.
Insights
Ubiquitination, a protein modification, is crucial in atherosclerosis development. Targeting E3 ligases, key players in ubiquitination, offers a new strategy to prevent this vascular disease.
Area of Science:
- Biochemistry
- Cardiovascular Biology
- Molecular Medicine
Background:
- Atherosclerosis is a major global cause of death, driven by complex molecular mechanisms.
- Key factors include abnormal lipid metabolism, inflammation, and cell dysfunction.
- The precise molecular pathways, especially post-translational modifications, are not fully understood.
Purpose of the Study:
- To review the role of ubiquitination in atherosclerosis pathogenesis.
- To highlight the contributions of E3 ligases in this vascular disease.
- To explore therapeutic potential of targeting E3 ligases.
Main Methods:
- Literature review focusing on ubiquitination and E3 ligases in atherosclerosis.
- Analysis of studies investigating molecular mechanisms of atherosclerosis.
- Synthesis of current knowledge on ubiquitin-modifying enzymes.
Main Results:
- Ubiquitination significantly impacts vascular inflammation and endothelial/smooth muscle cell function.
- It plays a role in lipid metabolism and atherosclerotic plaque stability.
- Various E3 ligases are implicated in the development of atherosclerosis.
Conclusions:
- Ubiquitination is a critical regulator in atherosclerosis.
- E3 ligases are key mediators in the disease's progression.
- Targeting E3 ligases presents a promising therapeutic avenue for atherosclerosis prevention.
Abstract:
Atherosclerosis is a chronic inflammatory vascular disease. Atherosclerotic cardiovascular disease is the main cause of death in both developed and developing countries. Many pathophysiological factors, including abnormal cholesterol metabolism, vascular inflammatory response, endothelial dysfunction and vascular smooth muscle cell proliferation and apoptosis, contribute to the development of atherosclerosis and the molecular mechanisms underlying the development of atherosclerosis are not fully understood. Ubiquitination is a multistep post-translational protein modification that participates in many important cellular processes. Emerging evidence suggests that ubiquitination plays important roles in the pathogenesis of atherosclerosis in many ways, including regulation of vascular inflammation, endothelial cell and vascular smooth muscle cell function, lipid metabolism and atherosclerotic plaque stability. This review summarizes important contributions of various E3 ligases to the development of atherosclerosis. Targeting ubiquitin E3 ligases may provide a novel strategy for the prevention of the progression of atherosclerosis.
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