Loading clinical trials...
Loading clinical trials...
Assessing the Expressions of Ezrin, Phosphorylated Ezrin, and Pip5k1α in the Airway Smooth Muscle of Asthmatic Patient
Asthma, a prevalent chronic respiratory affliction, significantly impinges upon the quality of life for affected individuals. Timely and appropriate diagnostic measures, coupled with efficacious therapeutic interventions, are paramount in mitigating exacerbations of symptoms and enhancing the life quality of patients. Ezrin plays an important role in maintaining cell morphology, cell migration, cell adhesion and polarisation, but Ezrin expression in airway smooth muscle remains unclear. Pip5k1α is an important kinase involved in intracellular phosphatidylinositol signalling pathways that may be involved in smooth muscle contraction and diastole. Therefore, further studies are necessary to elucidate the changes of Ezrin and Pip5k1α in patients with asthma to provide a basis for investigating alternative treatments for asthma.
Asthma is a complex and heterogeneous disease with a combination of genetic and environmental multifactors, which is mainly characterised by recurrent episodes of wheezing, shortness of breath, chest tightness and cough. The nature of the pathology manifests itself as a chronic inflammatory disease with abnormal antigen presentation and T-cell activation, and an imbalance of Th1/Th2 cells leading to dysfunction of airway smooth muscle cells. There is a lack of safe and effective medications against asthma for current treatment. For example, although glucocorticosteroids are the first-line drugs for asthma, only 12% of patients are able to use them in accordance with medical advice. β2 agonists are often used in combination with hormones, but up to 55% of asthmatics still fail to get effective control of their symptoms. Therefore, the development of innovative drugs with new targets and mechanisms has become the trend of asthma drug development at home and abroad. The discovery of new asthma targets will help to elucidate the asthma mechanism and solve a series of problems in clinical treatment. Ezrin is one of the major members of the Ezrin-Radixin-Moesin (ERM) family, which plays an important role in the maintenance of cell morphology, cell migration, cell adhesion and polarisation. Pip5k1α is an important kinase involved in the intracellular phosphatidylinositol signaling pathway, which may be associated with the smooth muscle contraction and diastole related. In a previous study, single-cell sequencing of lung tissue from asthmatic mice revealed that Ezrin and Pip5k1α were significantly increased in asthmatic airway smooth muscle cells. In vitro cellular experiments suggested that Ezrin and Pip5k1α inhibition could inhibit airway smooth muscle cell contraction, suggesting that inhibitors of both may provide a therapeutic advantage for reducing lung resistance in asthma. Therefore, further studies to elucidate the changes of Ezrin and Pip5k1α in asthma patients are warranted to provide a basis for the use of inhibitors of both as an alternative treatment for asthma.
Age
18 - 70 years
Sex
ALL
Healthy Volunteers
Yes
Yueyang Hospital, Shanghai University of Traditional Chinese Medicine
Shanghai, Shanghai Municipality, China
Start Date
May 28, 2024
Primary Completion Date
December 31, 2026
Completion Date
December 31, 2026
Last Updated
January 14, 2026
120
ESTIMATED participants
No intervention.
OTHER
Lead Sponsor
Lei-Miao Yin
Collaborators
NCT07219173
NCT07486401
Data Source & Attribution
This clinical trial information is sourced from ClinicalTrials.gov, a service of the U.S. National Institutes of Health.
Modifications: This data has been reformatted for display purposes. Eligibility criteria have been parsed into inclusion/exclusion sections. Location data has been geocoded to enable distance-based search. For the authoritative and most current information, please visit ClinicalTrials.gov.
Neither the United States Government nor Clareo Health make any warranties regarding the data. Check ClinicalTrials.gov frequently for updates.
View ClinicalTrials.gov Terms and ConditionsNCT02327897