The etiology of idiopathic pulmonary fibrosis (IPF) remains unknown, and therapeutic interventions are currently restricted. The activation of lung fibroblasts and the focal adhesion kinase (FAK) signaling pathway are crucial to the pathogenesis of IPF, yet the exact molecular mechanisms remain incompletely understood. Our study shows that the deleted in lymphocytic leukemia 2 (DLEU2) is elevated in the peripheral blood of patients with IPF, as well as in the lung tissues of mice with pulmonary fibrosis. Functional assays revealed that overexpression of DLEU2 facilitated fibrogenesis, whereas its suppression attenuated lung fibrosis in vivo and impeded fibroblast activation in vitro, predominantly through the regulation of FAK phosphorylation. Mechanistically, our findings reveal that DLEU2 regulates lung fibroblast activation by targeting miR-29a-3p. Conversely, inhibition of miR-29a-3p reversed the anti-fibrotic effects observed upon DLEU2 knockdown. Furthermore, DLEU2 was shown to directly interact with FAK, enhancing its phosphorylation and thereby facilitating fibrogenesis; inhibition of FAK phosphorylation counteracted the pro-fibrotic effects induced by DLEU2 overexpression. Taken together, these findings clarify the function of DLEU2 in facilitating FAK phosphorylation via its interactions with miR-29a-3p and FAK. The findings of this study suggest that DLEU2 may serve as a novel diagnostic biomarker and a potential therapeutic target for the treatment of IPF.

Single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST) have advanced the study of complex lung diseases by resolving cellular heterogeneity, tissue architecture, and intercellular communication. These technologies are particularly informative in chronic respiratory disorders, where pathological remodeling involves coordinated alterations across epithelial, stromal, immune, and endothelial compartments. Idiopathic pulmonary fibrosis (IPF), a rare fatal fibrotic disorder, and chronic obstructive pulmonary disease (COPD), a prevalent heterogeneous respiratory condition, represent distinct chronic lung diseases shaped by persistent injury, maladaptive repair, and progressive tissue remodeling. However, current understanding of their pathogenesis remains incomplete, and conventional approaches lack the resolution to define disease-associated cell states, spatially restricted niches, or compartment-specific interactions. This review synthesizes recent scRNA-seq and ST studies in IPF and COPD, emphasizing how high-resolution atlases refine established pathobiological frameworks and reveal shared and disease-specific cellular programs. We highlight epithelial dysfunction and impaired progenitor repair as shared mechanistic features of IPF and COPD, while emphasizing alveolar regenerative failure, fibroblast activation, and profibrotic niche formation as central features of IPF, and compartment-specific airway remodeling, inflammatory epithelial states, and emphysema-associated parenchymal injury as prominent features of COPD. We further discuss stromal and immune remodeling, hypoxia-associated vascular remodeling, and the translational implications of these findings for molecular stratification, target prioritization, and mechanism-informed therapeutic development, while noting limitations related to end-stage tissue sampling, platform constraints, and mouse-human correspondence. This review provides an integrated framework for understanding the cellular and spatial mechanisms underlying the pathogenesis and translational relevance of IPF and COPD.

Neonatal respiratory diseases remain a leading cause of morbidity and mortality in intensive care settings, with management complicated by the limitations of current monitoring tools. Chest radiography provides only static snapshots and cannot capture the dynamic evolution of lung aeration, while lung ultrasound, though portable, remains operator-dependent and incapable of quantifying regional ventilation. Electrical Impedance Tomography (EIT) has emerged as a noninvasive, radiation free imaging modality that addresses these gaps by enabling real time, continuous visualization of regional lung function at the bedside. This review synthesises evidence from studies published between 2011 and 2026, examining how EIT informs the management of neonatal respiratory distress syndrome, acute respiratory distress syndrome, bronchopulmonary dysplasia, pneumothorax, and the transitions inherent to mechanical ventilation. Across these disease contexts, EIT reveals regional ventilation heterogeneity invisible to conventional monitors, provides immediate physiological feedback during therapeutic interventions, and enables early detection of complications before clinical deterioration. We identify key barriers to clinical adoption, including technical limitations, lack of standardised protocols, and the need for outcome driven trials, and propose a research agenda to accelerate translation. By reframing EIT not merely as an imaging tool but as a dynamic decision support system integrated into clinical workflows, we aim to provide clinicians with a framework for leveraging this technology to improve outcomes in the most vulnerable patients.

This study explores the role of Sulfatase 1 (SULF1) in the progression of Chronic Obstructive Pulmonary Disease (COPD). SULF1, a modifying enzyme involved in various biological processes, was quantified in human serum using ELISA, and its correlation with lung function was analyzed. The in vivo function of SULF1 was investigated through CRISPR-mediated gene knockout (KO) in mice, and SULF1 overexpression was induced via adeno-associated virus (AAV). A COPD model was established by exposing mice to cigarette smoke (CS). Our findings revealed that SULF1 levels were elevated in the serum of COPD patients, where they negatively correlated with the FEV1/FVC ratio and the FEV1/FVC ratio annual decline. In CS-exposed mice, SULF1 expression was downregulated in lung tissues but increased in serum and bronchoalveolar lavage fluid (BALF). SULF1 KO mice exhibited more pronounced emphysematous changes following CS exposure, whereas SULF1 overexpression partially mitigated these lung alterations. Additionally, SULF1 was found to play a protective role in COPD progression through stable binding with Keratin 15 (KRT15). In conclusion, this study elucidates the role of SULF1 in COPD progression, providing novel insights into its pathogenesis and identifying potential therapeutic targets.