The Genome‐wide Landscape of Oxidative Base Damage in Hypoxia; Potential Role in Metabolic Reprogramming in Chronic Lung Disease

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Grant Daly ◽  
Dominika Houserova ◽  
Christopher Michael Francis ◽  
Joel Andrews ◽  
Raymond J. Langley ◽  
...  
2018 ◽  
Vol 132 (3) ◽  
pp. 375-379 ◽  
Author(s):  
Mathew Suji Eapen ◽  
Sukhwinder Singh Sohal

Airway infections are considered as one of the vital factors driving the pathophysiology of chronic lung disease with significant influences on disease trajectory. Opportunistic lung microbes in diseased conditions induce excessive exacerbations and contribute to airflow limitation. Though there has been considerable amount of information that ascertains their links with airway inflammation, the intricate interaction in clinical conditions are poorly understood and requires further deciphering. Current therapeutic interventions for such pathologies are few and lack the ability to modulate underlying dysfunctional immunity as well as suppress the excessive infectious conditions. Thus, in this Commentary we provide a focused outlook on the mechanisms involved in microbial infestation in lung diseases and provides important information on new therapeutic interventions including the potential role of Resolvins and their derivatives as alternative therapeutic agents in combating such multifaceted pathological mechanisms.


2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 750-750
Author(s):  
Victor Thannickal

Abstract The cause-effect relationships between the various “hallmarks of aging” and chronic lung disease are not well understood. We have determined overlapping pathways involving deregulated nutrient sensing, mitochondrial dysfunction, and cellular senescence that may contribute to the evolution of chronic lung disease. In particular, I will discuss alterations in energy/metabolic sensing pathways and mitochondrial dysfunction as pathobiological mechanisms that may explain the age-related increased susceptibility to the development and progression of idiopathic pulmonary fibrosis (IPF), a disease of pulmonary aging. I will then broaden the discussion to include the potential role of these biologic alterations in other chronic lung disease which burden older adults.


PEDIATRICS ◽  
2001 ◽  
Vol 108 (1) ◽  
pp. 212-214
Author(s):  
J. P. Shenai; ◽  
P. Rimensberger; ◽  
U. Thome ◽  
F. Pohlandt; ◽  
P. Rimensberger

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