個人簡歷

段軍超，首都醫科大學公共衛生學院，教授/博士生導師，國家重點研發計畫青年首席科學家，北京市傑出青年科學基金得主。主要從事顆粒物毒理學領域相關研究工作。近年來，先後主持國家及省級計畫10餘項，以第一作者或通訊作者在Biotechnol Adv，Biomaterials，Cardiovasc Res，Redox Biol，Part Fibre Toxicol等期刊發表SCI論文70餘篇。兼任中國毒理學會青年委員會副主任委員、中國毒理學會遺傳毒理學專業委員會副主任委員、中國毒理學會奈米毒理學專業委員會委員等，獲教育部自然科學獎一等獎一項。

Abstract

Chinese Title:

大氣細懸浮微粒對心肺系統的影響及其機制研究

English Title:

The effects and the mechanism of atmospheric fine particulate matter on cardiopulmonary system

Abstract

Air pollution has become one of the major global threats to public health. Fine particulate matter (PM2.5) can be deposited in the alveoli through respiration, penetrate the vascular walls, and enter the circulatory system, thereby increasing the risk of cardiovascular and pulmonary diseases as well as mortality. Mitochondrial dysfunction is considered a key mechanism underlying the adverse effects of air pollutants on the cardiopulmonary system.

Our research group has demonstrated that PM2.5 leads to inflammatory cell infiltration and collagen deposition in rat lungs, with mitochondrial oxidative stress and the resulting disruption of mitochondrial DNA homeostasis being key mechanisms driving PM2.5-induced pulmonary fibrosis in mice. Mitochondria-targeted antioxidants, such as MitoQ, effectively reduce reactive oxygen species production, enhance antioxidant defenses, and mitigate the progression of pulmonary fibrosis. In the cardiovascular system, PM2.5 has been shown to induce aortic fibrosis, increase vascular stiffness, and decrease elasticity in mice. It also promotes phenotypic changes in human aortic smooth muscle cells, mitochondrial oxidative damage, imbalances in mitochondrial dynamics, and activation of mitophagy. MitoQ intervention can significantly ameliorate these effects. Additionally, PM2.5 disrupts iron homeostasis in cardiomyocytes, causing excessive iron influx into mitochondria, which leads to redox imbalance, crosstalk between ferroptosis and mitophagy signaling pathways, ultimately resulting in mitochondrial dysfunction, myocardial hypertrophy, and cardiac dysfunction in mice. MitoQ, through its antioxidative properties, inhibits ferroptosis and protects against PM2.5-induced cardiotoxicity. These findings reveal key mechanisms by which PM2.5 damages the cardiopulmonary system and provide scientific evidence supporting the protective role of MitoQ in preventing and treating air pollution-related cardiopulmonary diseases.