Chapter Eight - Novel treatments against airway inflammation in COPD based on drug repurposing

Abstract

<p><a href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/chronic-obstructive-lung-disease" title="Learn more about Chronic obstructive pulmonary disease from ScienceDirect's AI-generated Topic Pages">Chronic obstructive pulmonary disease</a> (COPD) is a major cause of death and reduces quality of life that contributes to a health problem worldwide. Chronic <a href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/respiratory-tract-inflammation" title="Learn more about airway inflammation from ScienceDirect's AI-generated Topic Pages">airway inflammation</a> is a hallmark of COPD, which occurs in response to exposure of inhaled <a href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/irritant-agent" title="Learn more about irritants from ScienceDirect's AI-generated Topic Pages">irritants</a> like cigarette smoke. Despite accessible to the most up-to-date medications, none of the treatments is currently available to decrease the <a href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/disease-exacerbation" title="Learn more about disease progression from ScienceDirect's AI-generated Topic Pages">disease progression</a>. Therefore, it is believed that drugs which can reduce <a href="https://www.sciencedirect.com/topics/pharmacology-toxicology-and-pharmaceutical-science/respiratory-tract-inflammation" title="Learn more about airway inflammation from ScienceDirect's AI-generated Topic Pages">airway inflammation</a> will provide effective disease modifying therapy for COPD. There are many broad-range anti-inflammatory drugs including those that inhibit <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/signal-transduction" title="Learn more about cell signaling from ScienceDirect's AI-generated Topic Pages">cell signaling</a> pathways like inhibitors of p38 mitogen-activated protein kinase (MAPK), nuclear factor-κB (NF-κB), and phosphoinositide-3-kinase (PI3K), are now in phase III development for COPD. In this chapter, we review recent basic research data in the laboratory that may indicate novel therapeutic pathways arisen from currently used drugs such as selective monoamine oxidase (MAO)-B inhibitors and <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/drug-targeting" title="Learn more about drugs targeting from ScienceDirect's AI-generated Topic Pages">drugs targeting</a> peripheral <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/benzodiazepine" title="Learn more about benzodiazepine from ScienceDirect's AI-generated Topic Pages">benzodiazepine</a> receptors [also known as <a href="https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/translocator-protein" title="Learn more about translocator protein from ScienceDirect's AI-generated Topic Pages">translocator protein</a> (TSPO)] to reduce airway inflammation. Considering the impact of chronic airway inflammation on the lives of COPD patients, the potential pharmacological candidates for new anti-inflammatory targets should be further investigated. In addition, it is crucial to consider the phenotypes/molecular endotypes of COPD patients together with specific outcome measures to target novel therapies. This review will enhance our knowledge on how cigarette smoke affects MAO-B activity and TSPO activation/inactivation with specific ligands through regulation of mitochondrial function, and will help to identify new potential treatment for COPD in future.</p>