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The role and regulation of microRNAs in asthma

Ariel, Danit; Upadhyay, Daya

Current Opinion in Allergy and Clinical Immunology: February 2012 - Volume 12 - Issue 1 - p 49–52
doi: 10.1097/ACI.0b013e32834ecb7f
MECHANISMS OF ALLERGY AND ADULT ASTHMA: Edited by Stephen T. Holgate and J. Andrew Grant

Purpose of review Asthma is a common chronic inflammatory airway disorder that is characterized by variable and recurring airflow obstruction, chronic airway inflammation and bronchial hyper-responsiveness. The etiopathogenesis of asthma remains a complex issue. The intricacy in developing a more effective therapeutic strategy may be due to a large diversity in causative agents and a lack of understanding of the precise molecular mechanism involved in asthma. However, recent identification of microRNAs (miRs) has enhanced technological abilities to understand the disease process.

Recent findings miRs regulate gene expression by controlling the translation of a specific type of messenger RNA. miRs have been recently identified as key regulatory RNAs with immense significance in numerous biological processes including asthma. miRs have been implicated to have a fundamental role in acute and chronic asthma and in airway remodeling by the regulation of multiple signal transduction pathways that are involved in the pathogenesis of asthma. It is possible that miRs may bring a fundamental change to our understanding of the pathophysiology of asthma. This may then lead to the development of novel efficacious therapeutic strategies in asthma.

Summary In this review, we highlight the current understanding of the role and regulation of miRs in asthma.

aDivision of Pulmonary and Critical Care Medicine

bDivision of Endocrinology, Stanford University School of Medicine, Stanford, California, USA

Correspondence to Daya Upadhyay, MD, Assistant Professor, Division of Pulmonary and Critical Care Medicine, Stanford University School of Medicine, 300 Pasteur Drive, Room H3143, Stanford, CA 94305-5236, USA. Tel: +1 650 723 6381; fax: +1 650 725 5489; e-mail:

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