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Published on: February 20, 2019
Role of hyperhomocysteinemia in atherosclerosis: from bench to bedside
Wende Tian1,2, Jianqing Ju1, Baoyi Guan3
1National Clinical Research Center for Chinese Medicine Cardiology, Xiyuan Hospital, China Academy of Chinese Medical Sciences, Beijing China.
Insights
High homocysteine levels (HHcy) accelerate atherosclerosis through inflammation and oxidative stress. This review connects HHcy mechanisms to prevention and management strategies for this major cause of mortality.
Area of Science:
- Cardiovascular Science
- Metabolic Disease Research
- Vascular Biology
Background:
- Atherosclerosis is a primary global mortality driver.
- Hyperhomocysteinemia (HHcy) is a significant, modifiable risk factor.
- HHcy contributes to endothelial dysfunction, oxidative stress, and vascular inflammation.
Purpose of the Study:
- To review mechanisms of HHcy in atherosclerosis.
- To connect mechanistic insights with clinical applications.
- To discuss prevention and management strategies for HHcy-induced atherosclerosis.
Main Methods:
- Comprehensive literature review.
- Analysis of publications on HHcy and atherosclerosis.
- Examination of HHcy's role in atherogenesis.
Main Results:
- HHcy accelerates atherosclerosis via inflammation, oxidative stress, and epigenetic modification.
- Alterations in lipoprotein metabolism are implicated.
- HHcy is a contributing risk factor and an accelerator of atherogenic processes.
Conclusions:
- HHcy plays a complex role in atherosclerosis progression.
- This review consolidates recent advancements linking fundamental research to clinical practice.
- Understanding HHcy mechanisms is crucial for managing atherosclerosis.
Background:
Atherosclerosis is a leading cause of global mortality, driven by complex interactions between genetic, metabolic, and environmental factors. Among these, hyperhomocysteinemia (HHcy) has emerged as a significant and modifiable risk factor, contributing to endothelial dysfunction, oxidative stress, and vascular inflammation. Despite increasing recognition of its role in atherogenesis, the precise mechanisms and clinical implications of HHcy remain incompletely understood, necessitating a comprehensive review to connect recent mechanistic insights with practical applications.
Methods:
We analyzed the various mechanisms whereby HHcy accelerates the progression of atherosclerosis, and conducted a comprehensive review of publications in the fields of HHcy and atherosclerosis.
Results:
HHcy promotes atherosclerosis through several mechanisms, including inflammation, oxidative stress, epigenetic modification, and lipoprotein metabolism alteration. Moreover, this discussion extends to current strategies for the prevention and clinical management of HHcy-induced atherosclerosis.
Conclusion:
This review consolidates and elucidates the latest advancements and insights into the role of HHcy in atherosclerosis. The comprehensive narrative connects fundamental research with clinical applications. Contemporary studies highlight the complex interplay between HHcy and atherosclerosis, establishing HHcy as not only a contributing risk factor but also an accelerator of various atherogenic processes.
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