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p38 MAPK signaling in chronic obstructive pulmonary disease pathogenesis and inhibitor therapeutics.
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- المؤلفون: Ahmadi A;Ahmadi A; Ahrari S; Ahrari S; Salimian J; Salimian J; Salehi Z; Salehi Z; Karimi M; Karimi M; Emamvirdizadeh A; Emamvirdizadeh A; Jamalkandi SA; Jamalkandi SA; Ghanei M; Ghanei M
- المصدر:
Cell communication and signaling : CCS [Cell Commun Signal] 2023 Nov 02; Vol. 21 (1), pp. 314. Date of Electronic Publication: 2023 Nov 02.- نوع النشر :
Journal Article; Review; Systematic Review; Video-Audio Media- اللغة:
English - المصدر:
- معلومة اضافية
- المصدر: Publisher: BioMed Central Country of Publication: England NLM ID: 101170464 Publication Model: Electronic Cited Medium: Internet ISSN: 1478-811X (Electronic) Linking ISSN: 1478811X NLM ISO Abbreviation: Cell Commun Signal Subsets: MEDLINE
- بيانات النشر: Original Publication: [London] : BioMed Central, c2003-
- الموضوع:
- نبذة مختصرة : 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. Video Abstract.
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COPD. 2019 Dec;16(5-6):344-353. (PMID: 31682162) - Contributed Indexing: Keywords: COPD; COPD pharmacotherapy; Chronic Obstructive Pulmonary Disease; Systematic review; p38 MAPK inhibitors; p38 MAPK signaling
Local Abstract: [plain-language-summary] We wanted to determine what studies have been done on how a protein called p38 affects a lung disease called COPD. COPD is a condition that makes it hard to breathe and can cause coughing, wheezing, and chest infections. p38 is a protein that helps cells to respond to stress and inflammation, but it may also play a role in causing or worsening COPD. We searched two main online databases for studies that met our criteria. We looked for studies that involved humans, studies that used animals or cells in the lab, studies that reported new findings, studies that were written in English, and studies that focused on p38 and COPD. We did not include studies that were reviews, summaries, opinions, or letters or studies that were not related to p38 or COPD. We found 361 studies that matched our criteria. We read the titles and summaries of these studies and checked the full texts for quality and relevance. We collected information from each study, such as who did it, when and where it was done, how many people were involved, what type of cells were studied, what treatment was given, what outcome was measured, and what the main results were. We grouped the studies based on the type of cells and type of treatment they studied. We found that different types of cells (such as lung cells, immune cells, and blood cells) and different types of treatment can affect how p38 works in COPD. - الموضوع: Date Created: 20231103 Date Completed: 20231113 Latest Revision: 20231113
- الموضوع: 20231114
- الرقم المعرف: PMC10623820
- الرقم المعرف: 10.1186/s12964-023-01337-4
- الرقم المعرف: 37919729
- المصدر:
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