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Changes in diaphragm contractility in cigarette smoking-exposed and smoking cessation rats are associated with alterations in mitochondrial morphology and homeostasis

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机构: [1]Department of Emergency Medicine, Beijing Shijitan Hospital, Capital Medical University, Beijing, China [2]Department of Respiratory and Critical Care Medicine, Beijing Institute of Respiratory Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China [3]Department of Respiratory and Critical Care Medicine, Beijing Youan Hospital, Capital Medical University, Beijing, China [4]The Clinical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China [5]Department of Respiratory and Critical Care Medicine, Beijing Tongren Hospital, Capital Medical University, Beijing, China
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关键词: autophagy cigarette smoking diaphragm fission fusion mitochondrion

摘要:
The effects of cigarette smoking (CS) cessation on the diaphragm are unknown, as are the CS-induced diaphragmatic mitochondrial changes. We examined the changes in diaphragm contractility, as well as alterations in mitochondrial morphology, function and homoeostasis during CS exposure and after cessation. Rats were randomly divided into CS exposure and CS cessation groups: 3-month CS (S3), 6-month CS (S6), 6-month CS followed by 3-month cessation (S6N3). The changes in the diaphragm were investigated, including contractile properties, the ultrastructure, mitochondrial function and the expression of markers of mitochondrial homoeostasis. CS caused irreversible histological disruption and functional depression in the lungs, along with significantly declines in diaphragmatic contractility and more severely in extensor digitorum longus muscular contractility. Such declines were recovered after 3-month CS cessation. CS exposure disrupted the diaphragmatic mitochondrial morphology and function (S6), which was significantly alleviated in the S6N3 group. The mitochondrial homoeostasis was depressed (S6), as indicated by the downregulation of Pink1 and Mfn1. Interestingly, the Mfn1 level was recovered after smoking cessation (S6N3). In conclusion, smoking cessation eased CS-induced diaphragmatic dysfunction and mitochondrial deregulation, which are likely associated with deregulated mitochondrial homoeostasis.

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出版当年[2021]版:
大类 | 3 区 医学
小类 | 3 区 药学 3 区 毒理学
最新[2023]版:
大类 | 4 区 医学
小类 | 4 区 药学 4 区 毒理学
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出版当年[2020]版:
Q2 TOXICOLOGY Q2 PHARMACOLOGY & PHARMACY
最新[2023]版:
Q2 PHARMACOLOGY & PHARMACY Q3 TOXICOLOGY

影响因子: 最新[2023版] 最新五年平均 出版当年[2020版] 出版当年五年平均 出版前一年[2019版] 出版后一年[2021版]

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第一作者机构: [1]Department of Emergency Medicine, Beijing Shijitan Hospital, Capital Medical University, Beijing, China [2]Department of Respiratory and Critical Care Medicine, Beijing Institute of Respiratory Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China [3]Department of Respiratory and Critical Care Medicine, Beijing Youan Hospital, Capital Medical University, Beijing, China
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通讯作者:
通讯机构: [2]Department of Respiratory and Critical Care Medicine, Beijing Institute of Respiratory Medicine, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China [3]Department of Respiratory and Critical Care Medicine, Beijing Youan Hospital, Capital Medical University, Beijing, China [4]The Clinical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China [*1]The Clinical Research Center, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China. [*2]Department of Respiratory and Critical Care Medicine, Beijing Youan Hospital, Capital Medical University, Beijing, China.
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