Oxidative Stress-Induced Mitochondrial Dysfunction and Asthma

  • Samarpana Chakraborty
  • Kritika Khanna
  • Anurag AgrawalEmail author


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.


Allergic asthma Obese-asthma Mitochondrial dysfunction Oxidative stress Immune responses Epithelial barrier function Nitric oxide metabolism Lipoxygenase pathway Obesity Metabolic syndrome ADMA 





12-S-hydroxyeicosatetraenoic acid


13-S-hydroxyoctadecadienoic acid


Asymmetric dimethylarginine


Adenosine monophosphate


Adenosine triphosphate


Ca2+/calmodulin-dependent protein kinase II


C-type lectin receptors


Damage-associated molecular pattern


Dendritic cell


Dynamin-related protein 1


Endothelial nitric oxide synthase


Electron transport chain


2-Dihydro flavin adenine dinucleotide


House dust mite


Immunoglobulin E






Mitochondrial calcium uniporter


Metabolic syndrome


Major histocompatibility complex class II


Mesenchymal stem cell


Mitochondrial DNA


Nicotinamide adenine dinucleotide (reduced)


Nicotinamide adenine dinucleotide phosphate (reduced)


Nuclear DNA


Nuclear factor kappa-light-chain-enhancer of activated B cells


N-Formyl peptides


Nucleotide-binding domain/leucine-rich repeat receptor


Nod-like receptor family pyrin domain containing 3


Nitric oxide


Nuclear respiratory factor-1




Optic atrophy protein 1




Pathogen-associated molecular pattern


Peripheral blood mononuclear cells




Peroxisome proliferator-activated receptor-gamma coactivator


Protein kinase C delta type


Pyrroloquinoline quinone


Pathogen recognition receptor


Retinoic acid-inducible gene (RIG-1)-like receptors


Reactive oxygen species


Small interfering RNA


T-cell receptor


Mitochondrial transcription factor A


Type 2 T helper cells


Toll-like receptor


Tumour necrosis factor alpha


Transient receptor potential cation channel subfamily V member 1


Ubiquinol-cytochrome c reductase core protein II


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Copyright information

© Springer Nature Singapore Pte Ltd. 2020

Authors and Affiliations

  • Samarpana Chakraborty
    • 1
  • Kritika Khanna
    • 1
  • Anurag Agrawal
    • 1
    • 2
    • 3
    Email author
  1. 1.CSIR Institute of Genomics and Integrative BiologyDelhiIndia
  2. 2.Academy of Scientific and Innovative ResearchDelhiIndia
  3. 3.Baylor College of MedicineHoustonUSA

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