氧化应激是动脉粥样硬化性心血管疾病的临床、社会和遗传危险因素的基础

IF 2.3 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Emily Mewborn, Ansley Stanfill
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引用次数: 0

摘要

背景:动脉粥样硬化性心血管疾病(ASCVD)仍然是世界范围内死亡的主要原因,目前的风险评估工具很难预测。ASCVD危险因素与氧化应激(OS)相关的生物学机制以及氧化应激如何累积ASCVD风险被误解。目的:建立一个全面的概念模型,解释临床、社会和遗传ASCVD风险因素如何通过OS累积ASCVD风险。结论:OS(主要由过多的活性氧引起)和炎症存在于整个ASCVD病理生理连续统中。临床和社会ASCVD危险因素(包括高血压、肥胖、糖尿病、肾病、炎症性疾病、物质使用、营养不良、社会心理压力、空气污染、种族和遗传血统)的扩展列表主要通过增加OS影响ASCVD。许多风险因素发挥正反馈机制,增加OS。一种遗传风险因素,即触珠蛋白(Hp)基因型,与糖尿病患者ASCVD风险升高相关,并且假设由于Hp 2-2基因型增加OS而导致胰岛素抵抗的患者也存在同样的风险。意义:了解OS的生物学机制有助于了解这些ASCVD危险因素之间的相互关系以及复合ASCVD风险。个体化ASCVD风险评估应包括全面、整体的风险因素,以更好地解决OS的临床、社会和遗传影响。预防和减少OS是预防ASCVD发生或进展的关键。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease.

Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease.

Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease.

Oxidative Stress Underpins Clinical, Social, and Genetic Risk Factors for Atherosclerotic Cardiovascular Disease.

Background: Atherosclerotic cardiovascular disease (ASCVD) remains the leading cause of death worldwide and is poorly predicted with current risk estimation tools. The biological mechanisms relating ASCVD risk factors to oxidative stress (OS) and how this accumulates ASCVD risk are misunderstood.

Purpose: To develop a comprehensive conceptual model explaining how expanded clinical, social, and genetic ASCVD risk factors accumulate ASCVD risk through OS.

Conclusions: OS (primarily from excess reactive oxygen species) and inflammation are present along the entire ASCVD pathophysiologic continuum. An expanded list of clinical and social ASCVD risk factors (including hypertension, obesity, diabetes, kidney disease, inflammatory diseases, substance use, poor nutrition, psychosocial stress, air pollution, race, and genetic ancestry) influence ASCVD largely through increased OS. Many risk factors exert a positive feedback mechanism to increase OS. One genetic risk factor, haptoglobin (Hp) genotype, is associated with higher ASCVD risk in diabetes and hypothesized to do the same in those with insulin resistance due to the Hp 2-2 genotype increasing OS.

Implications: Understanding the biological mechanisms of OS informs how these ASCVD risk factors relate to each other and compound ASCVD risk. Individualized ASCVD risk estimation should include a comprehensive, holistic perspective of risk factors to better address the clinical, social, and genetic influences of OS. Preventing and reducing OS is key to preventing ASCVD development or progression.

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来源期刊
Clinical Medicine Insights. Cardiology
Clinical Medicine Insights. Cardiology CARDIAC & CARDIOVASCULAR SYSTEMS-
CiteScore
5.20
自引率
3.30%
发文量
16
审稿时长
8 weeks
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