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State of the Art in Pathogenesis and Targeted Therapy in...
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State of the Art in Pathogenesis and Targeted Therapy in Chronic Obstructive Pulmonary Disease

A special issue of Journal of Personalized Medicine (ISSN 2075-4426). This special issue belongs to the section "Personalized Therapy in Clinical Medicine".

Deadline for manuscript submissions: 30 August 2026 | Viewed by 810

Special Issue Editor

Dr. Emanuela Tudorache

E-Mail Website
Guest Editor
Center for Research and Innovation in Precision Medicine of Respiratory Diseases, “Victor Babes” University of Medicine and Pharmacy Timisoara, Eftimie Murgu Square 2, 300041 Timisoara, Romania
Interests: respiratory medicine; interstitial lung diseases; bronchoscopy; interventional pulmonology; chronic obstruc-tive pulmonary disease

Special Issue Information

Dear Colleagues,

Chronic obstructive pulmonary disease (COPD) is a leading cause of morbidity and mortality worldwide, posing significant challenges to healthcare systems.

This Special Issue will delve into the latest advances in understanding the pathogenesis of COPD and innovative approaches to its targeted therapy. It will cover a broad spectrum of topics, including, but not limited to, the molecular and genetic underpinnings of COPD, the role of inflammation in disease progression, novel biomarkers for diagnosis and prognosis, and the latest developments in treatment, mostly focused on targeted therapies. Furthermore, it will explore emerging trends in personalized medicine for COPD, novel drug delivery systems, and the challenges and barriers in translating research findings into clinical practice. Ultimately, this Special Issue will inspire further research and improve patient outcomes by advancing both scientific knowledge and clinical practice in COPD management.

We encourage all researchers, clinicians, and healthcare professionals with expertise in COPD to engage with this Special Issue. We welcome contributions that showcase emerging research, clinical practices, and novel perspectives in the diagnosis and management of COPD. By sharing new data and ideas, we can collectively advance this field and improve patient care.

Dr. Emanuela Tudorache
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Personalized Medicine is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • COPD
  • effective treatments
  • molecular
  • genetic
  • inflammation
  • biomarkers for diagnosis and prognosis
  • personalized medicine
  • novel drug delivery systems
  • patient outcomes
  • clinical practice

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  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
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Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

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Research

13 pages, 270 KB  
Article
Asthma-Associated COPD Etiotype: Clinical Features and Inflammatory Patterns in Biological Samples
by Camyla Fernandez de Farias, José Baddini-Martinez, Ana Luisa Godoy Fernandes, Maria Marta Amorim, Michel Dracoulakis, Maria Amélia Santos, Lilian Ballini Caetano and Fernando Sergio Leitão Filho
J. Pers. Med. 2025, 15(12), 615; https://doi.org/10.3390/jpm15120615 - 10 Dec 2025
Viewed by 506
Abstract
Background: The Global Initiative for Chronic Obstructive Lung Disease (GOLD) recognizes asthma as a potential causal pathway for chronic obstructive pulmonary disease, referred to as the COPD-A etiotype. However, the clinical and inflammatory characteristics of this phenotype remain poorly defined. Objectives: [...] Read more.
Background: The Global Initiative for Chronic Obstructive Lung Disease (GOLD) recognizes asthma as a potential causal pathway for chronic obstructive pulmonary disease, referred to as the COPD-A etiotype. However, the clinical and inflammatory characteristics of this phenotype remain poorly defined. Objectives: This study aimed to characterize clinical traits and cytokine profiles in stable asthmatics exhibiting persistent airflow limitation compatible with COPD-A. Methods: In this cross-sectional study, 94 stable asthmatic patients (71.3% female; age = 54.0 ± 15.6 years) without relevant smoking or environmental exposures were evaluated. COPD-A was defined by a post-bronchodilator FEV1/FVC ratio < 0.70. Asthma control (ACQ, ACT), quality of life (AQLQ), and lung function were assessed. Levels of IL-5, IL-8, IL-13, IL-17A, IL-17F, IL-25, IL-33, and TNF were quantified in nasal lavage, induced sputum, and blood samples. Results: Among the participants, 42 (44.7%) fulfilled COPD-A criteria. Compared with non-COPD-A subjects, those with COPD-A were older (60.5 vs. 48.7 years; p < 0.001) and had longer disease duration (39.8 vs. 30.1 years; p < 0.001), lower post-bronchodilator FEV1% predicted (68.1 vs. 87.1%; p < 0.001), and poorer asthma control (ACQ = 1.00 vs. 0.64; p = 0.003). Cytokine levels were comparable between groups except for higher IL-8 concentrations in induced sputum of COPD-A subjects (7.66 vs. 2.51 pg/mL; p = 0.024). Sputum IL-8 ≥ 3.096 pg/mL independently predicted COPD-A (aOR = 12.82; p = 0.023). Conclusions: Over 40% of non-smoking asthmatics exhibited persistent airflow limitation consistent with COPD-A. Elevated sputum IL-8 levels may be a potential biomarker of this etiotype. Full article
(This article belongs to the Special Issue State of the Art in Pathogenesis and Targeted Therapy in Chronic Obstructive Pulmonary Disease)
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