The critical role of epigenetic mechanism in PM_2.5-induced cardiovascular diseases.

IF 2.7 4区医学 Q2 GENETICS & HEREDITY

Genes and Environment Pub Date : 2021-10-15 DOI:10.1186/s41021-021-00219-w

Qinglin Sun, Xiaoke Ren, Zhiwei Sun, Junchao Duan

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引用次数: 14

Abstract

Cardiovascular disease (CVD) has become the leading cause of death worldwide, which seriously threatens human life and health. Epidemiological studies have confirmed the occurrence and development of CVD are closely related to air pollution. In particular, fine particulate matter (PM_2.5) is recognized as an important environmental factor contributing to increased morbidity, mortality and hospitalization rates among adults and children. However, the underlying mechanism by which PM_2.5 promotes CVD development remains unclear. With the development of epigenetics, recent studies have shown that PM_2.5 exposure may induce or aggravate CVD through epigenetic changes. In order to better understand the potential mechanisms, this paper reviews the epigenetic changes of CVD caused by PM_2.5. We summarized the epigenetic mechanisms of PM_2.5 causing cardiovascular pathological damage and functional changes, mainly involving DNA methylation, non-coding RNA, histone modification and chromosome remodeling. It will provide important clues for exploring the biological mechanisms affecting cardiovascular health.

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表观遗传机制在pm2.5诱导的心血管疾病中的关键作用。

心血管疾病(CVD)已成为世界范围内主要的死亡原因，严重威胁着人类的生命和健康。流行病学研究证实，心血管疾病的发生和发展与空气污染密切相关。特别是，细颗粒物(PM2.5)被认为是导致成人和儿童发病率、死亡率和住院率上升的一个重要环境因素。然而，PM2.5促进心血管疾病发展的潜在机制尚不清楚。随着表观遗传学的发展，近年来的研究表明PM2.5暴露可能通过表观遗传改变诱发或加重CVD。为了更好地了解PM2.5引起CVD的潜在机制，本文综述了PM2.5引起CVD的表观遗传变化。我们总结了PM2.5引起心血管病理损伤和功能改变的表观遗传机制，主要涉及DNA甲基化、非编码RNA、组蛋白修饰和染色体重塑。这将为探索影响心血管健康的生物学机制提供重要线索。

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

Genes and Environment Biochemistry, Genetics and Molecular Biology-Genetics

CiteScore

4.00

自引率

0.00%

发文量

审稿时长

27 weeks

期刊介绍： Genes and Environment is an open access, peer-reviewed journal that aims to accelerate communications among global scientists working in the field of genes and environment. The journal publishes articles across a broad range of topics including environmental mutagenesis and carcinogenesis, environmental genomics and epigenetics, molecular epidemiology, genetic toxicology and regulatory sciences. Topics published in the journal include, but are not limited to, mutagenesis and anti-mutagenesis in bacteria; genotoxicity in mammalian somatic cells; genotoxicity in germ cells; replication and repair; DNA damage; metabolic activation and inactivation; water and air pollution; ROS, NO and photoactivation; pharmaceuticals and anticancer agents; radiation; endocrine disrupters; indirect mutagenesis; threshold; new techniques for environmental mutagenesis studies; DNA methylation (enzymatic); structure activity relationship; chemoprevention of cancer; regulatory science. Genetic toxicology including risk evaluation for human health, validation studies on testing methods and subjects of guidelines for regulation of chemicals are also within its scope.