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In asthma, the increase in airway smooth muscle (ASM) can contribute to inflammation, airway wall remodeling and airway hyperresponsiveness (AHR). Targetting peroxisome proliferator-activated receptor   γ   (PPAR  γ  ), a receptor upregulated in ASM in asthmatic airways, may provide a novel approach to regulate these contributions. This review summarises experimental evidence that PPAR  γ   ligands, such as rosiglitazone (RGZ) and pioglitazone (PGZ), inhibit proliferation and inflammatory cytokine production from ASM  in vitro . In addition, inhaled administration of these ligands reduces inflammatory cell infiltration and airway remodelling in mouse models of allergen-induced airways disease. PPAR  γ   ligands can also regulate ASM contractility, with acute treatment eliciting relaxation of mouse trachea  in vitro  through a PPAR  γ  -independent mechanism. Chronic treatment can protect against the loss of bronchodilator sensitivity to   β    2 -adrenoceptor agonists and inhibit the development of AHR associated with exposure to nicotine  in utero  or following allergen challenge. Of particular interest, a small clinical trial has shown that oral RGZ treatment improves lung function in smokers with asthma, a group that is generally unresponsive to conventional steroid treatment. These combined findings support further investigation of the potential for PPAR  γ   agonists to target the noncontractile and contractile functions of ASM to improve outcomes for patients with poorly controlled asthma.

PPARγLigands Regulate Noncontractile and Contractile Functions of Airway Smooth Muscle: Implications for Asthma Therapy