Effects of Dietary Restriction on PGC-1α Regulation in the Development of Age-associated Diseases.

Shefilyn Widjaja, R. Antarianto, N. Hardiany
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Abstract

Ageing is the most significant risk factor for a number of non-communicable diseases, manifesting as cognitive, metabolic, and cardiovascular diseases. Although multifactorial, mitochondrial dysfunction and oxidative stress have been proposed to be the driving forces of ageing. Peroxisome proliferator-activated receptor γ coactivator α (PGC-1α) is a transcriptional coactivator central to various metabolic functions, of which mitochondrial biogenesis is the most prominent function. Inducible by various stimuli, including nutrient limitations, PGC-1α is a molecule of interest in the maintenance of mitochondrial function and, therefore, the prevention of degenerative diseases. This review involves a literature search for articles retrieved from PubMed using PGC-1α, ageing, and dietary restriction as keywords. Dietary restriction has been shown to promote tissue-specific PGC-1α expression. Both dietary restriction and PGC-1α upregulation have been shown to prolong the lifespans of both lower and higher-level organisms; the incidence of non-communicable diseases also decreased in fasting mammals. In conclusion, dietary interventions may delay ageing by regulating healthy mitochondria in various organs, presenting the possibility of a new primary prevention for many age-related diseases.
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饮食限制对 PGC-1α 在老年相关疾病发展过程中的调节作用
老龄化是多种非传染性疾病的最主要风险因素,表现为认知、代谢和心血管疾病。线粒体功能障碍和氧化应激虽然是多因素的,但已被认为是老龄化的驱动力。过氧化物酶体增殖激活受体γ辅激活因子α(PGC-1α)是一种转录辅激活因子,对各种代谢功能起着核心作用,其中线粒体的生物生成功能最为突出。PGC-1α 可被包括营养限制在内的各种刺激诱导,是维持线粒体功能的重要分子,因此也是预防退行性疾病的重要分子。本综述以 PGC-1α、老龄化和饮食限制为关键词,对从 PubMed 上检索到的文章进行文献检索。研究表明,饮食限制可促进组织特异性 PGC-1α 的表达。研究表明,饮食限制和PGC-1α上调都能延长低等生物和高等生物的寿命;禁食哺乳动物的非传染性疾病发病率也有所下降。总之,饮食干预可通过调节各器官中健康的线粒体来延缓衰老,为许多与年龄有关的疾病提供了一种新的初级预防方法。
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来源期刊
Current aging science
Current aging science Medicine-Geriatrics and Gerontology
CiteScore
3.90
自引率
0.00%
发文量
40
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