Mitochondrial Damage and Hypertension: Another Dark Side of Sodium Excess.

IF 4.6 3区 医学 Q1 NUTRITION & DIETETICS Current Nutrition Reports Pub Date : 2023-09-01 DOI:10.1007/s13668-023-00486-9
Baris Afsar, Rengin Elsurer Afsar
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Abstract

Purpose of review: Essential or primary hypertension (HT) is a worldwide health problem with no definitive cure. Although the exact pathogenesis of HT is not known, genetic factors, increased renin-angiotensin and sympathetic system activity, endothelial dysfunction, oxidative stress, and inflammation play a role in its development. Environmental factors such as sodium intake are also important for BP regulation, and excess sodium intake in the form of salt (NaCl, sodium chloride) increases blood pressure in salt-sensitive people. Excess salt intake increases extracellular volume, oxidative stress, inflammation, and endothelial dysfunction. Recent evidence suggests that increased salt intake also disturbs mitochondrial function both structurally and functionally which is important as mitochondrial dysfunction is associated with HT. In the current review, we have summarized the experimental and clinical data regarding the impact of salt intake on mitochondrial structure and function.

Recent findings: Excess salt intake damage mitochondrial structure (e.g., shorter mitochondria with less cristae, increased mitochondrial fission, increased mitochondrial vacuolization). Functionally, high salt intake impairs mitochondrial oxidative phosphorylation and electron transport chain, ATP production, mitochondrial calcium homeostasis, mitochondrial membrane potential, and mitochondrial uncoupling protein function. Excess salt intake also increases mitochondrial oxidative stress and modifies Krebs cycle protein expressions. Studies have shown that high salt intake impairs mitochondrial structure and function. These maladaptive mitochondrial changes facilitate the development of HT especially in salt-sensitive individuals. High salt intake impairs many functional and structural components of mitochondria. These mitochondrial alterations along with increased salt intake promote the development of hypertension.

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线粒体损伤和高血压:钠过量的另一个阴暗面。
综述目的:原发性高血压(HT)是一种全球性的健康问题,没有明确的治疗方法。虽然HT的确切发病机制尚不清楚,但遗传因素、肾素-血管紧张素和交感神经系统活性增加、内皮功能障碍、氧化应激和炎症在其发展中起作用。环境因素如钠的摄入对血压调节也很重要,过量的钠以盐(NaCl,氯化钠)的形式摄入会增加盐敏感人群的血压。过量的盐摄入会增加细胞外体积、氧化应激、炎症和内皮功能障碍。最近的证据表明,盐摄入量增加也会在结构和功能上扰乱线粒体功能,这一点很重要,因为线粒体功能障碍与HT有关。在这篇综述中,我们总结了盐摄入对线粒体结构和功能影响的实验和临床数据。最近的研究发现:过量的盐摄入会损害线粒体结构(例如,线粒体变短,嵴减少,线粒体分裂增加,线粒体空泡化增加)。功能上,高盐摄入损害线粒体氧化磷酸化和电子传递链、ATP生成、线粒体钙稳态、线粒体膜电位和线粒体解偶联蛋白功能。过量的盐摄入也会增加线粒体氧化应激并改变克雷布斯循环蛋白的表达。研究表明,高盐摄入会损害线粒体的结构和功能。这些不适应的线粒体变化促进了HT的发展,特别是在盐敏感个体中。高盐摄入会损害线粒体的许多功能和结构成分。这些线粒体的改变以及盐摄入量的增加促进了高血压的发展。
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来源期刊
Current Nutrition Reports
Current Nutrition Reports Agricultural and Biological Sciences-Food Science
CiteScore
7.70
自引率
2.00%
发文量
59
期刊介绍: This journal aims to provide comprehensive review articles that emphasize significant developments in nutrition research emerging in recent publications. By presenting clear, insightful, balanced contributions by international experts, the journal intends to discuss the influence of nutrition on major health conditions such as diabetes, cardiovascular disease, cancer, and obesity, as well as the impact of nutrition on genetics, metabolic function, and public health. We accomplish this aim by appointing international authorities to serve as Section Editors in key subject areas across the field. Section Editors select topics for which leading experts contribute comprehensive review articles that emphasize new developments and recently published papers of major importance, highlighted by annotated reference lists. We also provide commentaries from well-known figures in the field, and an Editorial Board of more than 25 internationally diverse members reviews the annual table of contents, suggests topics of special importance to their country/region, and ensures that topics and current and include emerging research.
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