Impact of Lipid Oxidation Products on Inflammation and Insulin Resistance: A Focus on Mechanisms of Action.

IF 2.5 4区 生物学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Tahar Hajri, Khadija Ouguerram, Thomas V Fungwe
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引用次数: 0

Abstract

The global rise in metabolic diseases, including obesity, diabetes, and cardiovascular diseases, has reached alarming levels, making them a major public health concern. Despite etiological heterogeneity, these maladies converge upon a triad of interrelated pathophysiological disturbances: chronic oxidative stress, lipid peroxidation, and sustained inflammatory responses. These dysregulated biological processes collectively underscore metabolic dysfunction; however, whether they work independently or as part of a cascade of mechanistic events is still under discussion. Oxidative stress, characterized by a disequilibrium between the generation of reactive oxygen species and endogenous antioxidative defense mechanisms, plays a pivotal role in the initiation and progressive deterioration of metabolic homeostasis. Likewise, lipid peroxidation engenders bioactive lipid derivatives that instigate cellular insult and perpetuate pro-inflammatory signaling cascades. Given the intricate molecular interplay among these pathophysiological processes, we conducted a comprehensive narrative synthesis to critically appraise the extant evidence about the causal interrelationships between lipid oxidation derivatives, inflammatory mediators, and oxidative stress. Specifically, our analysis aimed at elucidating the underlying mechanistic pathways through which lipid oxidation products modulate insulin signaling within myocytes, thereby influencing the functional integrity of both cardiac and skeletal muscle physiology.

脂质氧化产物对炎症和胰岛素抵抗的影响:作用机制的研究
包括肥胖、糖尿病和心血管疾病在内的全球代谢性疾病的增加已达到令人震惊的水平,使其成为一个主要的公共卫生问题。尽管病因异质性,这些疾病集中在一个三重相关的病理生理障碍:慢性氧化应激,脂质过氧化和持续的炎症反应。这些失调的生物过程共同强调了代谢功能障碍;然而,它们是独立工作还是作为一系列机制事件的一部分仍在讨论中。氧化应激以活性氧的产生与内源性抗氧化防御机制之间的不平衡为特征,在代谢稳态的开始和逐渐恶化中起着关键作用。同样,脂质过氧化产生具有生物活性的脂质衍生物,刺激细胞损伤并使促炎信号级联反应持续存在。鉴于这些病理生理过程之间复杂的分子相互作用,我们进行了全面的叙事综合,以批判性地评估关于脂质氧化衍生物、炎症介质和氧化应激之间因果关系的现有证据。具体来说,我们的分析旨在阐明脂质氧化产物调节肌细胞内胰岛素信号的潜在机制途径,从而影响心脏和骨骼肌生理学的功能完整性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Cell Biochemistry and Biophysics
Cell Biochemistry and Biophysics 生物-生化与分子生物学
CiteScore
4.40
自引率
0.00%
发文量
72
审稿时长
7.5 months
期刊介绍: Cell Biochemistry and Biophysics (CBB) aims to publish papers on the nature of the biochemical and biophysical mechanisms underlying the structure, control and function of cellular systems The reports should be within the framework of modern biochemistry and chemistry, biophysics and cell physiology, physics and engineering, molecular and structural biology. The relationship between molecular structure and function under investigation is emphasized. Examples of subject areas that CBB publishes are: · biochemical and biophysical aspects of cell structure and function; · interactions of cells and their molecular/macromolecular constituents; · innovative developments in genetic and biomolecular engineering; · computer-based analysis of tissues, cells, cell networks, organelles, and molecular/macromolecular assemblies; · photometric, spectroscopic, microscopic, mechanical, and electrical methodologies/techniques in analytical cytology, cytometry and innovative instrument design For articles that focus on computational aspects, authors should be clear about which docking and molecular dynamics algorithms or software packages are being used as well as details on the system parameterization, simulations conditions etc. In addition, docking calculations (virtual screening, QSAR, etc.) should be validated either by experimental studies or one or more reliable theoretical cross-validation methods.
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