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甲醛在心血管疾病和心脏发育中的细胞功能和分子机制。

The cellular function and molecular mechanism of formaldehyde in cardiovascular disease and heart development.

机构信息

Department of Cardiac Ultrasound, The Affiliated Hospital of Qingdao University, Qingdao, China.

Department of Immunology, Basic Medicine School, Qingdao University, Qingdao, China.

出版信息

J Cell Mol Med. 2021 Jun;25(12):5358-5371. doi: 10.1111/jcmm.16602. Epub 2021 May 10.

DOI:10.1111/jcmm.16602
PMID:33973354
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8184665/
Abstract

As a common air pollutant, formaldehyde is widely present in nature, industrial production and consumer products. Endogenous formaldehyde is mainly produced through the oxidative deamination of methylamine catalysed by semicarbazide-sensitive amine oxidase (SSAO) and is ubiquitous in human body fluids, tissues and cells. Vascular endothelial cells and smooth muscle cells are rich in this formaldehyde-producing enzyme and are easily damaged owing to consequent cytotoxicity. Consistent with this, increasing evidence suggests that the cardiovascular system and stages of heart development are also susceptible to the harmful effects of formaldehyde. Exposure to formaldehyde from different sources can induce heart disease such as arrhythmia, myocardial infarction (MI), heart failure (HF) and atherosclerosis (AS). In particular, long-term exposure to high concentrations of formaldehyde in pregnant women is more likely to affect embryonic development and cause heart malformations than long-term exposure to low concentrations of formaldehyde. Specifically, the ability of mouse embryos to effect formaldehyde clearance is far lower than that of the rat embryos, more readily allowing its accumulation. Formaldehyde may also exert toxic effects on heart development by inducing oxidative stress and cardiomyocyte apoptosis. This review focuses on the current progress in understanding the influence and underlying mechanisms of formaldehyde on cardiovascular disease and heart development.

摘要

作为一种常见的空气污染物,甲醛广泛存在于自然界、工业生产和消费品中。内源性甲醛主要通过半脒基敏感胺氧化酶(SSAO)催化的甲基胺的氧化脱氨产生,存在于人体的各种体液、组织和细胞中。血管内皮细胞和平滑肌细胞富含这种产生甲醛的酶,由于随之而来的细胞毒性而容易受到损伤。与此一致的是,越来越多的证据表明,心血管系统和心脏发育阶段也容易受到甲醛的有害影响。暴露于不同来源的甲醛可诱发心律失常、心肌梗死(MI)、心力衰竭(HF)和动脉粥样硬化(AS)等心脏病。特别是,孕妇长期暴露于高浓度甲醛比长期暴露于低浓度甲醛更可能影响胚胎发育并导致心脏畸形。具体来说,与大鼠胚胎相比,小鼠胚胎清除甲醛的能力要低得多,更容易使其积累。甲醛还可能通过诱导氧化应激和心肌细胞凋亡对心脏发育产生毒性作用。本综述重点介绍了目前对甲醛对心血管疾病和心脏发育影响及其潜在机制的理解进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/8184665/bbaf658a4468/JCMM-25-5358-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/8184665/5e1c13ff0297/JCMM-25-5358-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/8184665/63a003f90ec5/JCMM-25-5358-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/8184665/bbaf658a4468/JCMM-25-5358-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/8184665/5e1c13ff0297/JCMM-25-5358-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/8184665/63a003f90ec5/JCMM-25-5358-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8321/8184665/bbaf658a4468/JCMM-25-5358-g003.jpg

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