Special Issue "Genes, Mechanisms and Drugs for Asthma"

Guest Editor
Dr. P. Hemachandra Reddy
Neurogenetics Laboratory, Neuroscience Division, Oregon National Primate Research Center, West Campus, Oregon Health and Science University, 505 N.W., 185th Avenue Beaverton, OR 97006, USA
E-Mail: reddyh@ohsu.edu
Phone: +1 503 418 2625 (office); +1 503 418 2627 (lab)
Fax: +1 503 418 2501
Interests: aging; neurodegenerative diseases; gene expression analysis; transgenic mouse models; mitochondrial biology; mitochondrial function/dysfunction; mitochondrial therapeutics; mitochondrial dynamics

Dear Colleagues,

Asthma is a complex, inflammatory disorder characterized by airflow obstruction of variable degrees, bronchial hyper-responsiveness, and airway inflammation. Asthma is caused by environmental factors and a combination of genetic and environmental stimuli. Intense genetic studies in the last decade revealed that multiple genetic loci are involved in the etiology of asthma. Recent cellular, molecular, and animal model studies have revealed that several cellular events are involved in the progression of asthma, including: increased T-helper type 2 cytokines leading to the recruitment of inflammatory cells to the airway and, increased production of reactive oxygen species and mitochondrial dysfunction in the activated inflammatory cells, leading to tissue injury in the bronchial epithelium. The purpose of this issue is to assess the current status of research in asthma: 1) recent progress in genetic studies of asthma; 2) advances in cells/tissues from asthmatic humans, and induced animal models of allergic asthma; and 3) recent developments in therapeutics of asthma. This issue also discusses the current status of mitochondrial approaches in induced animal models of allergic asthma, and also in patients with asthma.

Dr. P. Hemachandra Reddy
Guest Editor

Submission

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• inflammation
• reactive oxygen species
• mitochondrial dysfunction
• oxidative stress
• antioxidant therapeutics
• allergic asthma
• airway inflammation