Divyaanka Iyer1, Navya Mishra2,3,4, Anurag Agrawal5,6. 1. CSIR Institute of Genomics and Integrative Biology, Delhi University campus, Mall Road, Delhi, 110007, India. 2. Indian Institute of Public Health, Gurugram, India. 3. Chest Research Foundation, Pune, India. 4. Academy of Scientific and Innovative Research, New Delhi, India. 5. CSIR Institute of Genomics and Integrative Biology, Delhi University campus, Mall Road, Delhi, 110007, India. a.agrawal@igib.in. 6. Academy of Scientific and Innovative Research, New Delhi, India. a.agrawal@igib.in.
Abstract
PURPOSE OF THE REVIEW: The connections between allergy, asthma and metabolic syndrome are becoming increasingly clear. Recent research suggests a unifying mitochondrial link between the diverse phenotypes of these interlinked morbidities. The scope of this review is to highlight cellular mechanisms, epidemiology and environmental allergens influencing mitochondrial function and its importance in allergy and asthma. We briefly also consider the potential of mitochondria-targeted therapies in prevention and cure. RECENT FINDINGS: Recent research has shown allergy, asthma and metabolic syndrome to be linked to mitochondrial dysfunction. Environmental pollutants and allergens are observed to cause mitochondrial dysfunction, primarily by inducing oxidative stress and ROS production. Malfunctioning mitochondria change the bioenergetics of the cell and its metabolic profile to favour systemic inflammation, which drives all three types of morbidities. Given the existing experimental evidence, approaches targeting mitochondria (e.g. antioxidant therapy and mitochondrial replacement) are being conducted in relevant disease models-with some progressing towards clinical trials, making mitochondrial function the focus of translational therapy research in asthma, allergy and linked metabolic syndrome.
PURPOSE OF THE REVIEW: The connections between allergy, asthma and metabolic syndrome are becoming increasingly clear. Recent research suggests a unifying mitochondrial link between the diverse phenotypes of these interlinked morbidities. The scope of this review is to highlight cellular mechanisms, epidemiology and environmental allergens influencing mitochondrial function and its importance in allergy and asthma. We briefly also consider the potential of mitochondria-targeted therapies in prevention and cure. RECENT FINDINGS: Recent research has shown allergy, asthma and metabolic syndrome to be linked to mitochondrial dysfunction. Environmental pollutants and allergens are observed to cause mitochondrial dysfunction, primarily by inducing oxidative stress and ROS production. Malfunctioning mitochondria change the bioenergetics of the cell and its metabolic profile to favour systemic inflammation, which drives all three types of morbidities. Given the existing experimental evidence, approaches targeting mitochondria (e.g. antioxidant therapy and mitochondrial replacement) are being conducted in relevant disease models-with some progressing towards clinical trials, making mitochondrial function the focus of translational therapy research in asthma, allergy and linked metabolic syndrome.
Entities:
Keywords:
Air pollution; Allergy; Asthma; Metabolic syndrome; Mitochondrial dysfunction; Mitochondrial transfer therapy; Systemic inflammation
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