Cellular stress responses and dysfunctional Mitochondrial–cellular senescence, and therapeutics in chronic respiratory diseases
Autor: | Hitendra S. Chand, Marko Manevski, Hoshang J. Unwalla, Isaac K. Sundar, Thivanka Muthumalage, Irfan Rahman, Qixin Wang, Kameshwar P. Singh, Dinesh Devadoss |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
0301 basic medicine
Clinical Biochemistry UPR Mitochondrion Bioinformatics medicine.disease_cause Cellular senescence Biochemistry Article 03 medical and health sciences Pulmonary Disease Chronic Obstructive 0302 clinical medicine Fibrosis Pulmonary fibrosis medicine COPD Humans Lung lcsh:QH301-705.5 DAMPs lcsh:R5-920 business.industry Organic Chemistry Cigarette smoke ROS medicine.disease Mitochondria Oxidative Stress 030104 developmental biology Cell metabolism medicine.anatomical_structure lcsh:Biology (General) Signal transduction business Mitochondrial dysfunction lcsh:Medicine (General) 030217 neurology & neurosurgery Oxidative stress |
Zdroj: | Redox Biology, Vol 33, Iss, Pp-(2020) Redox Biology |
ISSN: | 2213-2317 |
Popis: | The abnormal inflammatory responses due to the lung tissue damage and ineffective repair/resolution in response to the inhaled toxicants result in the pathological changes associated with chronic respiratory diseases. Investigation of such pathophysiological mechanisms provides the opportunity to develop the molecular phenotype-specific diagnostic assays and could help in designing the personalized medicine-based therapeutic approaches against these prevalent diseases. As the central hubs of cell metabolism and energetics, mitochondria integrate cellular responses and interorganellar signaling pathways to maintain cellular and extracellular redox status and the cellular senescence that dictate the lung tissue responses. Specifically, as observed in chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis, the mitochondria-endoplasmic reticulum (ER) crosstalk is disrupted by the inhaled toxicants such as the combustible and emerging electronic nicotine-delivery system (ENDS) tobacco products. Thus, the recent research efforts have focused on understanding how the mitochondria-ER dysfunctions and oxidative stress responses can be targeted to improve inflammatory and cellular dysfunctions associated with these pathologic illnesses that are exacerbated by viral infections. The present review assesses the importance of these redox signaling and cellular senescence pathways that describe the role of mitochondria and ER on the development and function of lung epithelial responses, highlighting the cause and effect associations that reflect the disease pathogenesis and possible intervention strategies. |
Databáze: | OpenAIRE |
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