Oxidative Stress-Induced Mitochondrial Dysfunction and Asthma

Abstract

Asthma is a well-recognized global concern with ever-increasing prevalence and economic burden worldwide. Genetic susceptibility and exposure to environmental triggers such as allergens, pollutants, infectious agents and even lifestyle choices are well-established modulators of the disease. Recent studies show that irrespective of the nature of causal trigger (allergic or nonallergic), mitochondria and its dysfunction is a central player in asthma pathogenesis. This chapter discusses the studies and mechanisms through which mitochondria plays its role in causing asthma pathogenesis. Under allergic asthma conditions, immune response and epithelial barrier functions are the key players modulating the function of mitochondria. Other mechanism that leads to the development of obese-asthma phenotype involves disruption of cellular bioenergetics via modulating nitric oxide levels, calcium homeostasis, etc. Repair, reprogramming and/or replacement of the dysfunctional mitochondria are some of the possible therapeutic strategies for better management of asthma.