线粒体稳态在 D-半乳糖诱导的心血管老化中的作用--从工作台到床边。

IF 3.9 3区 生物学 Q2 CELL BIOLOGY
Yogita Sahu, Pratiksha Jamadade, Krushna Ch Maharana, Sanjiv Singh
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引用次数: 0

摘要

衰老是一种不可避免的现象,它会随着时间的推移影响到从细胞到机体的各个层面。氧化应激和炎症现在被广泛认为是衰老过程中的关键过程,它们可能对线粒体 DNA 造成重大伤害,导致细胞凋亡。正常的循环功能是预测无病预期寿命的重要指标。事实上,影响心血管系统的疾病越来越常见,是全球发病率、残疾率和死亡率的主要原因。心血管衰老可能先于或可能支撑着与年龄相关的整体健康衰退。大量研究发现,软骨机制在衰老的发生和发展过程中发挥着至关重要的作用。D-半乳糖(D-gal)诱导衰老模型是公认的衰老研究常用模型。在这篇综述中,我们重新阐述了以前和现在关于线粒体稳态及其在 D-半乳糖心血管衰老中潜在机制的研究。此外,我们还重点介绍了应对导致心血管老化的主要并发症的新型治疗策略。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Role of mitochondrial homeostasis in D-galactose-induced cardiovascular ageing from bench to bedside

Ageing is an inevitable phenomenon which affects the cellular to the organism level in the progression of the time. Oxidative stress and inflammation are now widely regarded as the key processes involved in the aging process, which may then cause significant harm to mitochondrial DNA, leading to apoptosis. Normal circulatory function is a significant predictor of disease-free life expectancy. Indeed, disorders affecting the cardiovascular system, which are becoming more common, are the primary cause of worldwide morbidity, disability, and mortality. Cardiovascular aging may precede or possibly underpin overall, age-related health decline. Numerous studies have found mitochondrial mechanistc approach plays a vital role in the in the onset and development of aging. The D-galactose (D-gal)-induced aging model is well recognized and commonly used in the aging study. In this review we redeposit the association of the previous and current studies on mitochondrial homeostasis and its underlying mechanisms in D-galactose cardiovascular ageing. Further we focus the novel and the treatment strategies to combat the major complication leading to the cardiovascular ageing.

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来源期刊
Mitochondrion
Mitochondrion 生物-细胞生物学
CiteScore
9.40
自引率
4.50%
发文量
86
审稿时长
13.6 weeks
期刊介绍: Mitochondrion is a definitive, high profile, peer-reviewed international research journal. The scope of Mitochondrion is broad, reporting on basic science of mitochondria from all organisms and from basic research to pathology and clinical aspects of mitochondrial diseases. The journal welcomes original contributions from investigators working in diverse sub-disciplines such as evolution, biophysics, biochemistry, molecular and cell biology, genetics, pharmacology, toxicology, forensic science, programmed cell death, aging, cancer and clinical features of mitochondrial diseases.
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