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Biology
Special Issues
The Molecular and Cellular Mechanisms of Lung Injury and Recovery
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The Molecular and Cellular Mechanisms of Lung Injury and Recovery

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

Deadline for manuscript submissions: 30 September 2026 | Viewed by 1640

Special Issue Editors

Dr. Weiguo Chen

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Guest Editor
Department of Medicine, Division of Pulmonary, Critical Care, Sleep & Allergy, University of Illinois Chicago, Chicago, IL 60612, USA
Interests: acute lung injury; chronic lung injury; ARDS; fibrosis; allergy; mechanisms; therapy; infection; inflammation; endothelial barrier
Prof. Dr. Honglong Ji

E-Mail Website
Guest Editor
Department of Surgery, Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA
Interests: acute lung injury; chronic lung injury; ARDS; fibrosis; allergy; mechanisms; therapy; infection; inflammation; endothelial barrier
Dr. Ibra S. Fancher

E-Mail Website
Guest Editor
Department of Biological Sciences, College of Arts and Sciences, University of Delaware, Newark, DE, USA
Interests: acute lung injury; chronic lung injury; ARDS; fibrosis; allergy; mechanisms; therapy; infection; inflammation; endothelial barrier

Special Issue Information

Dear Colleagues,

Lung injury, caused by a variety of factors, remains a leading cause of death worldwide, yet its underlying mechanisms are still poorly understood. During the onset of acute lung injury, significant alterations occur in alveolar structure, including disruption of the endothelial–epithelial barrier and infiltration of inflammatory cells and protein-rich fluid into the alveolar spaces. These pathological changes compromise the lung’s capacity for oxygen–carbon dioxide exchange and can progress to acute respiratory distress syndrome (ARDS). In the recovery phase, injured lung cells may undergo apoptosis or regeneration, processes regulated by multiple molecular pathways.

In contrast to acute lung injury, chronic challenges—such as immune dysregulation, hypoxia, or chemical exposures—can lead to lung fibrosis, pulmonary emphysema, or pulmonary hypertension.

A better understanding of the molecular and cellular mechanisms driving these processes will aid in improving outcomes for patients with both acute and chronic lung injuries.

We welcome original research articles, reviews, and short communications that explore the molecular, cellular, and translational aspects of lung injury and repair. Contributions that provide new insights into the mechanisms of acute and chronic lung injury, highlight potential therapeutic targets, or advance our understanding of disease progression and recovery are especially encouraged. Submissions addressing innovative experimental models, biomarkers, or clinical applications are also highly valued.

Dr. Weiguo Chen
Prof. Dr. Honglong Ji
Dr. Ibra S. Fancher
Guest Editors

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. Biology is an international peer-reviewed open access semimonthly 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 2700 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

  • acute lung injury
  • chronic lung injury
  • ARDS
  • fibrosis
  • allergy
  • mechanisms
  • therapy
  • infection
  • inflammation
  • endothelial barrier

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Published Papers (2 papers)

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Research

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16 pages, 2207 KB  
Article
Local Lung HIF-1α and VEGF Activation to Reverse Emphysema by a Sulfated Caffeic Acid Dehydropolymer
by Tien M. Truong, Meghan L. Thompson, Umesh R. Desai and Masahiro Sakagami
Biology 2026, 15(7), 564; https://doi.org/10.3390/biology15070564 - 1 Apr 2026
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Abstract
In emphysema, the alveolar septal structure is progressively destroyed, which is believed to be irreversible. However, as it has recently been linked to vascular endothelial growth factor (VEGF) deficiency, we hypothesized that VEGF stimulation can promote lung cell proliferation/migration to reverse emphysema. Our [...] Read more.
In emphysema, the alveolar septal structure is progressively destroyed, which is believed to be irreversible. However, as it has recently been linked to vascular endothelial growth factor (VEGF) deficiency, we hypothesized that VEGF stimulation can promote lung cell proliferation/migration to reverse emphysema. Our sulfated caffeic acid dehydropolymer, CDSO3, was thus examined in vitro and in vivo, given its VEGF-stimulating activity via ferrous ion (Fe2+) chelation-mediated stabilization of hypoxia-inducible factor-1α (HIF-1α). In lung epithelial/endothelial cells, CDSO3 promoted proliferation and wound closure by 1.6–3.0-fold at 10 μM; however, these effects were negated by excess FeSO4 or an HIF-1α inhibitor, indicating an Fe2+- and HIF-1α-dependent mechanism. In rat models of established emphysema induced by cigarette smoke extract or the VEGF receptor antagonist SU5416, two-week lung administration of CDSO3 at 60 μg/kg from day 21 enabled: 68–79% recovery of exercise endurance and airspace enlargement/destruction; a 1.8-fold increase in proliferating cell nuclear antigen above healthy levels; normalization of cleaved caspase-3; restoration of HIF-1α; and a 1.3-fold increase in VEGF above healthy levels. In contrast, CDSO3 pre-chelated with Fe2+ was ineffective. In conclusion, Fe2+ chelation-mediated HIF-1α stabilization and VEGF stimulation via local lung delivery of CDSO3 can reverse established emphysema by promoting cell growth and survival. Full article
(This article belongs to the Special Issue The Molecular and Cellular Mechanisms of Lung Injury and Recovery)
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Review

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15 pages, 822 KB  
Review
Oxidative Stress as a Mechanistic Link Between Severe Respiratory Viral Infection and Pulmonary Fibrosis
by Shynggys Sergazy, Alexander Gulyaev and Zarina Shulgau
Biology 2026, 15(7), 556; https://doi.org/10.3390/biology15070556 - 31 Mar 2026
Viewed by 758
Abstract
Post-viral pulmonary fibrosis represents a clinically significant and mechanistically complex consequence of severe respiratory infection. The COVID-19 pandemic has highlighted that a subset of survivors, particularly those with severe pneumonia or acute respiratory distress syndrome, develop persistent fibrosis-like lung abnormalities, including reticulation and [...] Read more.
Post-viral pulmonary fibrosis represents a clinically significant and mechanistically complex consequence of severe respiratory infection. The COVID-19 pandemic has highlighted that a subset of survivors, particularly those with severe pneumonia or acute respiratory distress syndrome, develop persistent fibrosis-like lung abnormalities, including reticulation and traction bronchiectasis, often accompanied by impaired gas transfer. Although the clinical course is heterogeneous and many lesions regress over time, longitudinal studies indicate that structural and functional impairment may persist for years in susceptible individuals. Oxidative stress has emerged as a plausible convergent mechanism linking acute epithelial injury, dysregulated inflammatory resolution, and chronic fibrotic remodeling. Reactive oxygen and nitrogen species amplify inflammatory signaling, promote epithelial cell death and senescence, influence macrophage polarization, and activate canonical profibrotic pathways, notably the TGF-β axis. Redox imbalance is embedded within reinforcing circuits involving NOX4-dependent ROS amplification, mitochondrial dysfunction, endoplasmic reticulum stress, inflammasome activation, and senescence-associated secretory programs. Persistent immune activation and organelle stress may sustain redox dysregulation beyond viral clearance, thereby bridging acute lung injury to maladaptive remodeling. This review integrates epidemiological, clinical, and mechanistic evidence to position oxidative stress as a central mediator of post-viral lung fibrosis and discusses therapeutic and translational implications. Full article
(This article belongs to the Special Issue The Molecular and Cellular Mechanisms of Lung Injury and Recovery)
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