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   role of epigenetics in the pathogenesis of asthma  
   
نویسنده alizadeh zahra ,mortaz esmaeil ,adcock ian ,moin mostafa
منبع iranian journal of allergy, asthma and immunology - 2017 - دوره : 16 - شماره : 2 - صفحه:82 -91
چکیده    Asthma is a complex, heterogeneous and chronic airway inflammatory disease with different clinical phenotypes caused by diverse triggers and pathophysiological mechanisms. asthma heritability has been established in many genetic studies but it is evident that only genetic elements are not responsible for the development of asthma. increasing rate of asthma incidence during past decades has implicated the role of epigenetics in development of asthma. environmental factors perform as initiator signals through epigenetic mechanisms. three epigenetic mechanisms have been identified, including dna methylation, histone modifications, and small noncoding rnas. these mechanisms regulate the immune responses and inflammatory genes expression in asthma and allergy. this review explains the role of epigenetic modifications in controlling th2 response and ige production in asthma and also briefly overviews the role of environmental factors such as pollutions, allergens, prenatal exposures and diet in developing asthma. recognizing environmental risk factors and their effects on epigenetic mechanisms would be of great interest for prognostic and preventive aspect in treatment of asthma.
کلیدواژه asthma ,dna methylation ,epigenetics ,histone modification ,mirna ,environmental factors
آدرس tehran university of medical sciences, asthma and allergy research institute, ایران, shahid beheshti university of medical sciences, faculty of medicine, national research institute of tuberculosis and lung diseases (nritld), clinical tuberculosis and epidemiology research center, department of immunology, ایران, imperial college london, national heart and lung institute, airway disease section, uk, tehran university of medical sciences, asthma and allergy research institute, ایران
پست الکترونیکی mmoin@sina.yums.ac.ir
 
     
   
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