Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
9.0
4.9
Journals
IJMS
Special Issues
Novel Insights into Molecular Mechanisms of Pulmonary Pathology
Due to scheduled maintenance work on our servers, there may be short service disruptions on this website between 11:00 and 12:00 CEST on March 28th.
ijms-logo
Submit to IJMS Review for IJMS Propose a Special Issue

Journal Menu

► Journal Menu

Journal Browser

► Journal Browser
share announcement

Novel Insights into Molecular Mechanisms of Pulmonary Pathology

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 January 2026) | Viewed by 5829

Special Issue Editor

Dr. Qiaozhen Liu

E-Mail Website
Guest Editor
Massachusetts General Hospital, Center for Regenerative Medicine, 185 Cambridge Street, Boston, MA 02114, USA
Interests: pulmonary disease

Special Issue Information

Dear Colleagues,

The pulmonary system comprises one of the most vital systems in the human body, playing a crucial role in gas exchange and mucosal barrier integrity. Pathological conditions affecting the pulmonary system can have severe consequences. Diseases such as pneumonia, chronic obstructive pulmonary disease (COPD), idiopathic pulmonary fibrosis (IPF), asthma, pulmonary fibrosis, and, most importantly, lung cancer can lead to significantly compromised lung function, a shortened lifespan, and, if not adequately managed, result in death. These diseases stem from various causes, including acute or chronic infections (bacterial, viral, and fungal), exposure to environmental pollutants (such as tobacco smoke, occupational exposures, and air pollution), genetic predispositions, and immune system dysfunctions. The underlying mechanisms of these pulmonary diseases often involve an intricate interplay between genetic, epigenetic, and environmental factors. A comprehensive understanding of the molecular mechanisms of pulmonary pathology is crucial for improving the clinical detection of and developing therapeutic interventions for pulmonary diseases.

In this Special Issue, we invite any reviews, research articles, and case reports regarding the molecular mechanisms of any of the aforementioned pulmonary diseases. Join us in advancing the field by shedding light on the molecular intricacies of pulmonary diseases in this Special Issue.

Dr. Qiaozhen Liu
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • fibrosis
  • infection
  • COPD
  • asthma
  • IPF
  • pneumonia
  • lung cancer
  • molecular mechanism

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

19 pages, 75008 KB  
Article
ARPC2 Promotes Pulmonary Fibrosis by Regulating MRTFA Activity Independent of the Canonical ARP2/3 Complex
by Eun Jo Du, Hyunseong Kim, Seo-Gyeong Bae, Sihyeon An and Kanghyun Ryoo
Int. J. Mol. Sci. 2026, 27(6), 2729; https://doi.org/10.3390/ijms27062729 - 17 Mar 2026
Viewed by 409
Abstract
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease characterized by the pathological accumulation of collagen-rich extracellular matrix, resulting in irreversible lung remodeling and respiratory failure. The incomplete understanding of IPF pathogenesis has hindered the development of effective therapeutics. Here, we investigate [...] Read more.
Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive lung disease characterized by the pathological accumulation of collagen-rich extracellular matrix, resulting in irreversible lung remodeling and respiratory failure. The incomplete understanding of IPF pathogenesis has hindered the development of effective therapeutics. Here, we investigate the mechanism by which the actin-related protein 2/3 complex subunit 2 (ARPC2) contributes to the fibrotic response in lung fibroblasts. Modulating of ARPC2 expression levels altered the expression of profibrotic genes, including α-smooth muscle actin (ACTA2), in TGF-β1-treated MRC-5 cells at the transcriptional level. We further show that ARPC2 regulates the TGF-β1-mediated nuclear translocation of myocardin-related transcription factor-A (MRTFA), a central driver of fibrotic gene induction. Our data indicate that ARPC2 plays a distinct role in profibrotic gene expression and MRTFA nuclear localization, distinguishing its function from other components of the actin-related protein 2/3 (ARP2/3) complex. Furthermore, ARPC2 appears to modulate the TGF-β1-dependent formation of MRTFA/G-actin complexes. Finally, transcriptomic analysis of cells depleted of ARPC2, ACTR2, or MRTFA revealed that ARPC2 and MRTFA co-regulate a specific repertoire of fibrotic genes. These observations support a profibrotic function for ARPC2 during fibroblast-to-myofibroblast transition (FMT), highlighting it as a potential therapeutic target for IPF. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms of Pulmonary Pathology)
►▼ Show Figures

Figure 1

17 pages, 3031 KB  
Article
miR-30d Levels Predict Re-Hospitalization in Patients with Acute Cardiogenic Pulmonary Edema: A Preliminary Study
by Giordano Bianchi, Barbara Vizio, Ornella Bosco, Martina Schiavello, Paolo Cagna Vallino, Francesca Rumbolo, Fulvio Morello, Giulio Mengozzi, Giuseppe Montrucchio, Enrico Lupia and Emanuele Pivetta
Int. J. Mol. Sci. 2025, 26(3), 1278; https://doi.org/10.3390/ijms26031278 - 1 Feb 2025
Viewed by 1377
Abstract
Acute cardiogenic pulmonary edema (ACPE) is a common and serious manifestation of heart failure (HF), representing 10–20% of all acute HF admissions. It is associated with elevated in-hospital mortality and high rates of re-hospitalization. MicroRs, like miR-30d, are of particular interest in heart [...] Read more.
Acute cardiogenic pulmonary edema (ACPE) is a common and serious manifestation of heart failure (HF), representing 10–20% of all acute HF admissions. It is associated with elevated in-hospital mortality and high rates of re-hospitalization. MicroRs, like miR-30d, are of particular interest in heart failure due to their regulatory role in gene expression and potential as biomarkers for diagnosing and predicting patient outcomes, especially in high-risk cases such as ACPE. We conducted a cohort study on patients diagnosed with ACPE in the Emergency Department (ED). The circulating levels of miR-30d were analyzed at the time of hospital admission and at one-month follow-up along with other biomarkers. We enrolled 24 ACPE patients and 10 control subjects. Median age was 80.8 years (interquartile range, IQR, 8.2) in ACPE cases, and 78.5 years (IQR 9.8) in controls with a male/female ratio of 2 and 0.66, respectively. In ACPE patients, median cardiac ejection fraction was 42.5%, creatinine 1.63 mg/dL (IQR 1.24), troponin 63.5 ng/dL (58), and NT-proBNP 4243.5 pg/mL (IQR 5846) at ED evaluation. Median concentration of miR30d was 0.81 in controls, and 3.67 and 7.28 in ACPE patients at enrollment time and one month later, respectively. Re-hospitalization occurred in 7 ACPE patients in the following 3 months, and in 9 during the following year. miR-30d had a significant predictive value in assessing the risk of re-hospitalization at both 3 months and 1 year following the initial diagnosis of ACPE, while it did not in assessing the risk of death at 1 year. When compared with the other biomarkers, none of them showed a better accuracy than miR-30d. Our findings suggest that elevated levels of miR-30d are associated with an increased rate of hospital readmission at both 3 months and 1 year after discharge. Larger, multicenter studies will be needed to confirm the validity of circulating miR-30d levels as a potential biomarker useful for risk prediction in ACPE patients and its utility in improving individualized patient care. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms of Pulmonary Pathology)
►▼ Show Figures

Figure 1

Review

Jump to: Research

27 pages, 2417 KB  
Review
HIF-1α Pathway in COVID-19: A Scoping Review of Its Modulation and Related Treatments
by Felipe Paes Gomes da Silva, Rafael Matte, David Batista Wiedmer, Arthur Paes Gomes da Silva, Rafaela Makiak Menin, Fernanda Bressianini Barbosa, Thainá Aymê Mocelin Meneguzzi, Sabrina Barancelli Pereira, Amanda Terres Fausto, Larissa Klug, Bruna Pinheiro Melim and Claudio Jose Beltrão
Int. J. Mol. Sci. 2025, 26(9), 4202; https://doi.org/10.3390/ijms26094202 - 28 Apr 2025
Cited by 3 | Viewed by 3349
Abstract
The COVID-19 pandemic, driven by SARS-CoV-2, has led to a global health crisis, highlighting the virus’s unique molecular mechanisms that distinguish it from other respiratory pathogens. It is known that the Hypoxia-Inducible Factor 1α (HIF-1α) activates a complex network of intracellular signaling pathways [...] Read more.
The COVID-19 pandemic, driven by SARS-CoV-2, has led to a global health crisis, highlighting the virus’s unique molecular mechanisms that distinguish it from other respiratory pathogens. It is known that the Hypoxia-Inducible Factor 1α (HIF-1α) activates a complex network of intracellular signaling pathways regulating cellular energy metabolism, angiogenesis, and cell survival, contributing to the wide range of clinical manifestations of COVID-19, including Post-Acute COVID-19 Syndrome (PACS). Emerging evidence suggests that dysregulation of HIF-1α is a key driver of systemic inflammation, silent hypoxia, and pathological tissue remodeling in both the acute and post-acute phases of the disease. This scoping review was conducted following PRISMA-ScR guidelines and registered in INPLASY. It involved a literature search in Scopus and PubMed, supplemented by manual reference screening, with study selection facilitated by Rayyan software. Our analysis clarifies the dual role of HIF-1α, which may either worsen inflammatory responses and viral persistence or support adaptive mechanisms that reduce cellular damage. The potential for targeting HIF-1α therapeutically in COVID-19 is complex, requiring further investigation to clarify its precise role and translational applications. This review deepens the molecular understanding of SARS-CoV-2-induced cellular and tissue dysfunction in hypoxia, offering insights for improving clinical management strategies and addressing long-term sequelae. Full article
(This article belongs to the Special Issue Novel Insights into Molecular Mechanisms of Pulmonary Pathology)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-3
Back to TopTop