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Redox Homeostasis in Pulmonary Disorders

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (28 February 2021) | Viewed by 2871

Special Issue Editor

Department of Internal Medicine, School of Medicine Texas Tech University Health Sciences Center, Lubbock, TX 790430, USA
Interests: lung injury and repair; oxygen toxicity in the lung; pulmonary mitochondrial dysfunction in hyperoxia; redox signaling in lung injury and inflammation; bronchopulmonary dysplasia; oxidative lung diseases and molecular mechanisms

Special Issue Information

The lung is the only organ that directly communicates with the environment due to inhalation of ambient air for oxygenation. Although oxygen breathing is the very essence of living, oxygen is a major oxidizing agent in the body that oxidizes various biological molecules. Additionally, metabolism of oxygen in the pulmonary mitochondria produces reactive oxygen species that are potent oxidizers as well. Along with oxygen, we also breathe pollutants, allergens, both biological and chemical, and other toxic environmental particulates and gases. Further, the lung directly receives 20–21% oxygen in its alveoli compared to other organs in the body in which oxygen levels vary from 2% to 10%. Thus, the lung is designed to withstand significant oxidative insult compared to other organs. However, chronic exposure of the lung to various pathogens, toxic chemicals, allergens, and toxic gases promotes pulmonary disorders due to loss of redox homeostasis, resulting in enhanced pulmonary oxidative burden. The focus of this Special Issue is to present cutting-edge research in our current understanding of the impact of redox homeostasis in initiation and propagation of pulmonary disorders and the underlying cellular and molecular signaling mechanism associated with breathing of oxygen, environmental pollutants, allergens, microorganisms, and its impact on pulmonary defense system to lessen this chronic environmental insult. Further, the mechanisms by which loss of redox homeostasis might impact pathophysiology of the lung will also be addressed in this Special Issue.

Dr. Kumuda C Das
Guest Editor

Manuscript Submission Information

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Keywords

  • redox mechanisms
  • lung injury
  • COPD (chronic obstructive pulmonary disease)
  • ARDS (acute respiratory distress syndrome)
  • environmental toxicants and lung injury
  • lung mitochondria and redox
  • lung redox signaling
  • bronchopulmonary dysplasia (BPD)
  • lung inflammation and redox signaling

Published Papers (1 paper)

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Research

16 pages, 4379 KiB  
Article
Astragalin Inhibits Cigarette Smoke-Induced Pulmonary Thrombosis and Alveolar Inflammation and Disrupts PAR Activation and Oxidative Stress-Responsive MAPK-Signaling
by Yun-Ho Kim, Min-Kyung Kang, Eun-Jung Lee, Dong Yeon Kim, Hyeongjoo Oh, Soo-Il Kim, Su Yeon Oh, Woojin Na, Jae-Hoon Shim, Il-Jun Kang and Young-Hee Kang
Int. J. Mol. Sci. 2021, 22(7), 3692; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22073692 - 01 Apr 2021
Cited by 14 | Viewed by 2512
Abstract
Epidemiological evidence shows that smoking causes a thrombophilic milieu that may play a role in the pathophysiology of chronic obstructive pulmonary disease (COPD) as well as pulmonary thromboembolism. The increased nicotine level induces a prothrombotic status and abnormal blood coagulation in smokers. Since [...] Read more.
Epidemiological evidence shows that smoking causes a thrombophilic milieu that may play a role in the pathophysiology of chronic obstructive pulmonary disease (COPD) as well as pulmonary thromboembolism. The increased nicotine level induces a prothrombotic status and abnormal blood coagulation in smokers. Since several anticoagulants increase bleeding risk, alternative therapies need to be identified to protect against thrombosis without affecting hemostasis. Astragalin is a flavonoid present in persimmon leaves and green tea seeds and exhibits diverse activities of antioxidant and anti-inflammation. The current study investigated that astragalin attenuated smoking-induced pulmonary thrombosis and alveolar inflammation. In addition, it was explored that molecular links between thrombosis and inflammation entailed protease-activated receptor (PAR) activation and oxidative stress-responsive mitogen-activated protein kinase (MAPK)-signaling. BALB/c mice were orally administrated with 10–20 mg/kg astragalin and exposed to cigarette smoke for 8 weeks. For the in vitro study, 10 U/mL thrombin was added to alveolar epithelial A549 cells in the presence of 1–20 µM astragalin. The cigarette smoking-induced the expression of PAR-1 and PAR-2 in lung tissues, which was attenuated by the administration of ≥10 mg/kg astragalin. The oral supplementation of ≥10 mg/kg astragalin to cigarette smoke-challenged mice attenuated the protein induction of urokinase plasminogen activator, plasminogen activator inhibitor-1and tissue factor, and instead enhanced the induction of tissue plasminogen activator in lung tissues. The astragalin treatment alleviated cigarette smoke-induced lung emphysema and pulmonary thrombosis. Astragalin caused lymphocytosis and neutrophilia in bronchoalveolar lavage fluid due to cigarette smoke but curtailed infiltration of neutrophils and macrophages in airways. Furthermore, this compound retarded thrombin-induced activation of PAR proteins and expression of inflammatory mediators in alveolar cells. Treating astragalin interrupted PAR proteins-activated reactive oxygen species production and MAPK signaling leading to alveolar inflammation. Accordingly, astragalin may interrupt the smoking-induced oxidative stress–MAPK signaling–inflammation axis via disconnection between alveolar PAR activation and pulmonary thromboembolism. Full article
(This article belongs to the Special Issue Redox Homeostasis in Pulmonary Disorders)
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