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P38 Mapk Signaling in Chronic Obstructive Pulmonary Disease Pathogenesis and Inhibitor Therapeutics Publisher Pubmed



Ahmadi A1 ; Ahrari S2 ; Salimian J3 ; Salehi Z4 ; Karimi M5 ; Emamvirdizadeh A6 ; Jamalkandi SA7 ; Ghanei M7
Authors
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Authors Affiliations
  1. 1. Molecular Biology Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran
  2. 2. Department of Biochemistry and Molecular Medicine, Institute for Research in Immunology and Cancer (IRIC), Universite de Montreal, Montreal, QC, Canada
  3. 3. Applied Virology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
  4. 4. Hematology-Oncology and Stem Cell Transplantation Research Center, Tehran University of Medical Sciences, Tehran, Iran
  5. 5. Department of Traditional Medicine, School of Persian Medicine, Tehran University of Medical Sciences, Tehran, Iran
  6. 6. Department of Molecular Genetics, Faculty of Bio Sciences, Tehran North Branch, Islamic Azad University, Tehran, Iran
  7. 7. Chemical Injuries Research Center, Systems Biology and Poisonings Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran

Source: Cell Communication and Signaling Published:2023


Abstract

Background: Chronic obstructive pulmonary disease (COPD) is characterized by persistent respiratory symptoms and airflow limitation due to airway and/or alveolar remodeling. Although the abnormalities are primarily prompted by chronic exposure to inhaled irritants, maladjusted and self-reinforcing immune responses are significant contributors to the development and progression of the disease. The p38 isoforms are regarded as pivotal hub proteins that regulate immune and inflammatory responses in both healthy and disease states. As a result, their inhibition has been the subject of numerous recent studies exploring their therapeutic potential in COPD. Main body: We performed a systematic search based on the PRISMA guidelines to find relevant studies about P38 signaling in COPD patients. We searched the PubMed and Google Scholar databases and used “P38” AND “COPD” Mesh Terms. We applied the following inclusion criteria: (1) human, animal, ex vivo and in vitro studies; (2) original research articles; (3) published in English; and (4) focused on P38 signaling in COPD pathogenesis, progression, or treatment. We screened the titles and abstracts of the retrieved studies and assessed the full texts of the eligible studies for quality and relevance. We extracted the following data from each study: authors, year, country, sample size, study design, cell type, intervention, outcome, and main findings. We classified the studies according to the role of different cells and treatments in P38 signaling in COPD. Conclusion: While targeting p38 MAPK has demonstrated some therapeutic potential in COPD, its efficacy is limited. Nevertheless, combining p38 MAPK inhibitors with other anti-inflammatory steroids appears to be a promising treatment choice. Clinical trials testing various p38 MAPK inhibitors have produced mixed results, with some showing improvement in lung function and reduction in exacerbations in COPD patients. Despite these mixed results, research on p38 MAPK inhibitors is still a major area of study to develop new and more effective therapies for COPD. As our understanding of COPD evolves, we may gain a better understanding of how to utilize p38 MAPK inhibitors to treat this disease. [MediaObject not available: see fulltext.]. © 2023, The Author(s).
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