Molecular Mechanisms and New Targets of Refractory Asthma

A special issue of Biology (ISSN 2079-7737). This special issue belongs to the section "Biochemistry and Molecular Biology".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 1402

Special Issue Editors


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Guest Editor
Department of Pharmacology and Neuroscience, Creighton University School of Medicine, Omaha, NE 68124, USA
Interests: pharmacology; asthma; cancer biology; signal transduction; G-protein coupled receptor

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Guest Editor
Department of Pharmacology, Rutgers-Robert Wood Johnson Medical School, The State University of New Jersey, New Brunswick, NJ 08091, USA
Interests: biophysics; airway smooth muscle; lung diseases
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Special Issue Information

Dear Colleagues,

Asthma is a chronic obstructive inflammatory airway disease with substantial morbidity and mortality, affecting over 300 million people worldwide. Airway hyperresponsiveness and airway inflammation are hallmarks of asthma clinically managed with β2-agonist bronchodilators and corticosteroids. Refractory asthma manifests with persistent symptoms despite the use of high-dose corticosteroids and long-acting β2-agonists, leading to increased morbidity and costs associated with treatment. Understanding the mechanisms and developing strategies to overcome this therapeutic resistance pose a significant unmet need.

For this Special Issue, “Molecular Mechanisms and New Targets of Refractory Asthma”, we welcome the submission of original articles and reviews that explore all biological aspects of refractory asthma, with an emphasis on molecular mechanisms and new therapeutic targets. The goal of this Special Issue is to improve our understanding of the therapeutic resistance in asthma, and provide valuable insights to address the overarching challenge of refractory asthma.

Prof. Dr. Yaping Tu
Prof. Dr. Steven S. An
Guest Editors

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Keywords

  • refractory asthma
  • airway hyperresponsiveness
  • T2 and non-T2 inflammation
  • steroid resistance
  • therapeutic targets

Published Papers (1 paper)

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Review

12 pages, 456 KiB  
Review
Rho-Kinase Inhibition of Active Force and Passive Tension in Airway Smooth Muscle: A Strategy for Treating Airway Hyperresponsiveness in Asthma
by Yuto Yasuda, Lu Wang, Pasquale Chitano and Chun Y. Seow
Biology 2024, 13(2), 115; https://doi.org/10.3390/biology13020115 - 11 Feb 2024
Viewed by 1191
Abstract
Rho-kinase inhibitors have been identified as a class of potential drugs for treating asthma because of their ability to reduce airway inflammation and active force in airway smooth muscle (ASM). Past research has revealed that, besides the effect on the ASM’s force generation, [...] Read more.
Rho-kinase inhibitors have been identified as a class of potential drugs for treating asthma because of their ability to reduce airway inflammation and active force in airway smooth muscle (ASM). Past research has revealed that, besides the effect on the ASM’s force generation, rho-kinase (ROCK) also regulates actin filament formation and filament network architecture and integrity, thus affecting ASM’s cytoskeletal stiffness. The present review is not a comprehensive examination of the roles played by ROCK in regulating ASM function but is specifically focused on passive tension, which is partially determined by the cytoskeletal stiffness of ASM. Understanding the molecular basis for maintaining active force and passive tension in ASM by ROCK will allow us to determine the suitability of ROCK inhibitors and its downstream enzymes as a class of drugs in treating airway hyperresponsiveness seen in asthma. Because clinical trials using ROCK inhibitors in the treatment of asthma have yet to be conducted, the present review focuses on the in vitro effects of ROCK inhibitors on ASM’s mechanical properties which include active force generation, relaxation, and passive stiffness. The review provides justification for future clinical trials in the treatment of asthma using ROCK inhibitors alone and in combination with other pharmacological and mechanical interventions. Full article
(This article belongs to the Special Issue Molecular Mechanisms and New Targets of Refractory Asthma)
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