Airway remodeling: a potential therapeutic target in asthma

Zhang, Weixi; Li, Changchong

doi:10.1007/s12519-011-0264-x

Cited by 29 publications

(18 citation statements)

References 37 publications

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“…It has been reported that more than 300 million people worldwide suffer from asthma and this figure is predicted to increase by another 100 million by 2025 (3). A study highlighted that the prevalence of asthma increased remarkably in the past two decades, especially in children (4).…”

Section: Introductionmentioning

confidence: 99%

PTEN gene silencing contributes to airway remodeling and induces airway smooth muscle cell proliferation in mice with allergic asthma

Wen¹,

Yan²,

Han³

et al. 2018

J. Thorac. Dis.

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Section: Introductionmentioning

confidence: 99%

PTEN gene silencing contributes to airway remodeling and induces airway smooth muscle cell proliferation in mice with allergic asthma

Wen¹,

Yan²,

Han³

et al. 2018

J. Thorac. Dis.

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“…The primary therapeutic option for asthma is to address the imbalance between Th1 and Th2 cytokines such as interleukin (IL)-4, IL-5, and IL-13 [2,3]. Although the severity of this disease is definitively dependent on the extent of airway remodeling [4], including subepithelial fibrosis, mucous hypersecretion, extracellular matrix (ECM) deposition, increased airway smooth muscle (ASM) mass, and vascular alterations [5,6], little attention has been paid to anti-remodeling as a cure for asthma. Glucocorticoids are the first-line agents for asthma patients, owning to their therapeutic effects against airway inflammation and remodeling.…”

Section: Introductionmentioning

confidence: 99%

Effect of diosmetin on airway remodeling in a murine model of chronic asthma

Ge¹,

Liu²,

Zeng³

et al. 2015

ABBS

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Bronchial asthma, one of the most common allergic diseases, is characterized by airway hyperresponsiveness (AHR), inflammation, and remodeling. The anti-oxidant flavone aglycone diosmetin ameliorates the inflammation in pancreatitis, but little is known about its impact on asthma. In this study, the effects of diosmetin on chronic asthma were investigated with an emphasis on the modulation of airway remodeling in BALB/c mice challenged with ovalbumin (OVA). It was found that diosmetin significantly relieved inflammatory cell infiltration, goblet cell hyperplasia, and collagen deposition in the lungs of asthmatic mice and notably reduced AHR in these animals. The OVAinduced increases in total cell and eosinophil counts in bronchoalveolar lavage fluid were reversed, and the level of OVA-specific immunoglobulin E in serum was attenuated by diosmetin administration, implying an anti-Th2 activity of diosmetin. Furthermore, diosmetin remarkably suppressed the expression of smooth muscle actin alpha chain, indicating a potent anti-proliferative effect of diosmetin on airway smooth muscle cells (ASMCs). Matrix metallopeptidase-9, transforming growth factor-β1, and vascular endothelial growth factor levels were also alleviated by diosmetin, suggesting that the remission of airway remodeling might be attributed to the decline of these proteins. Taken together, our findings provided a novel profile of diosmetin with anti-remodeling therapeutic benefits, highlighting a new potential of diosmetin in remitting the ASMC proliferation in chronic asthma.

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“…Although there has been considerable progress in our understanding of the pathophysiology of asthma, the prevention and treatment of airway remodelling still constitute a significant problem. To date, long‐term medication in asthma treatment mainly focuses on anti‐inflammatory effects and there are no therapeutic interventions that can reverse established remodelling of the airways (Zhang and Li, ). AVE 0991 (AVE) is a synthetic compound that is a mimic of Ang‐(1–7) and is considered an agonist at Mas receptors (Wiemer et al ., ; Santos and Ferreira, ).…”

Section: Introductionmentioning

confidence: 99%

AVE 0991, a non‐peptide mimic of angiotensin‐(1–7) effects, attenuates pulmonary remodelling in a model of chronic asthma

Rodrigues-Machado

Magalhães

Cardoso

et al. 2013

British J Pharmacology

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BACKGROUND AND PURPOSEAVE 0991 (AVE) is a non-peptide compound, mimic of the angiotensin (Ang)-(1-7) actions in many tissues and pathophysiological states. Here, we have investigated the effect of AVE on pulmonary remodelling in a murine model of ovalbumin (OVA)-induced chronic allergic lung inflammation. EXPERIMENTAL APPROACHWe used BALB/c mice (6-8 weeks old) and induced chronic allergic lung inflammation by OVA sensitization (20 μg·mouse −1 , i.p., four times, 14 days apart) and OVA challenge (1%, nebulised during 30 min, three times per·week, for 4 weeks). Control and AVE groups were given saline i.p and challenged with saline. AVE treatment (1 mg·kg −1 ·per day, s.c.) or saline (100 μL·kg −1 ·per day, s.c.) was given during the challenge period. Mice were anaesthetized 72 h after the last challenge and blood and lungs collected. In some animals, primary bronchi were isolated to test contractile responses. Cytokines were evaluated in bronchoalveolar lavage (BAL) and lung homogenates. KEY RESULTSTreatment with AVE of OVA sensitised and challenged mice attenuated the altered contractile response to carbachol in bronchial rings and reversed the increased airway wall and pulmonary vasculature thickness and right ventricular hypertrophy. Furthermore, AVE reduced IL-5 and increased IL-10 levels in the BAL, accompanied by decreased Ang II levels in lungs. CONCLUSIONS AND IMPLICATIONSAVE treatment prevented pulmonary remodelling, inflammation and right ventricular hypertrophy in OVA mice, suggesting that Ang-(1-7) receptor agonists are a new possibility for the treatment of pulmonary remodelling induced by chronic asthma.

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Airway remodeling: a potential therapeutic target in asthma

Cited by 29 publications

References 37 publications

PTEN gene silencing contributes to airway remodeling and induces airway smooth muscle cell proliferation in mice with allergic asthma

PTEN gene silencing contributes to airway remodeling and induces airway smooth muscle cell proliferation in mice with allergic asthma

Effect of diosmetin on airway remodeling in a murine model of chronic asthma

AVE 0991, a non‐peptide mimic of angiotensin‐(1–7) effects, attenuates pulmonary remodelling in a model of chronic asthma

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