American journal of physiology. Lung cellular and molecular physiology最新文献

{"title":"Effect of elexacaftor and bamocaftor on the metabolic and thermal stability of the F508del-CFTR protein in human airway epithelial cells.","authors":"Thomas Carrez, Sandra Mirval, Christine Barrault, Florian Devetter, Clarisse Vandebrouck, Frédéric Becq","doi":"10.1152/ajplung.00011.2025","DOIUrl":"10.1152/ajplung.00011.2025","url":null,"abstract":"<p><p>Trikafta (elexacaftor/tezacaftor/ivacaftor; ETI) is approved for cystic fibrosis (CF) patients with at least one F508del mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene or another responsive mutation based on in vitro data. However, the pharmacological effects of ETI on F508del-CFTR remain incompletely defined in vitro. To explore the mechanisms underlying Trikafta's clinical efficacy, we used primary bronchial epithelial cells from F508del homozygous patients and CFBE41o-cells expressing F508del-CFTR. We assessed CFTR maturation, turnover, chloride transport, and thermal stability under various ETI concentrations and treatment durations at physiological temperature using electrophysiology (Ussing chamber, patch-clamp) and biochemical assays. We found that ETI efficacy on F508del-CFTR is strongly influenced by both treatment duration and concentration. Reducing ETI from standard doses, i.e., E (3 µM), T (18 µM), and I (1 µM), to 33%, 11%, 3.3%, and 1.1% decreased function and maturation, but 33% retained most of the corrective effect. After 2 h of treatment, around 50% of the CFTR-dependent current was preserved, unlike in untreated cells. Notably, replacing elexacaftor with bamocaftor further improved F508del-CFTR maturation and function compared with ETI, though it did not affect the rate of current decline over time. These findings highlight the importance of optimizing ETI dose and exposure duration, as both significantly affect F508del-CFTR stability and function. The retained efficacy at reduced concentrations suggests possible individualized dosing strategies, particularly for patients experiencing adverse effects with full-dose ETI.<b>NEW & NOTEWORTHY</b> Our in vitro study underscores that ETI/BTI's efficacy in improving F508del-CFTR function depends on treatment concentration and duration, impacting the protein's metabolic and thermal stability. Although ETI/BTI only partially addresses F508del-CFTR's inherent thermal instability, reduced doses retained significant effectiveness. This finding supports dose optimization as a promising strategy to sustain therapeutic benefits while minimizing side effects, offering a personalized approach to treatment for individuals with cystic fibrosis experiencing adverse effects from standard dosing.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L583-L597"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144843999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation of inflammatory lung injury and repair by transforming growth factors.","authors":"Mrinmay Chakrabarti, Mollie Phillips, Rana Dhar, Ansley Herron, Jason L Kubinak, Kiesha Wilson, E Angela Murphy, Mohamad Azhar, Colin E Evans","doi":"10.1152/ajplung.00154.2025","DOIUrl":"10.1152/ajplung.00154.2025","url":null,"abstract":"<p><p>Acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) are inflammatory conditions with substantial rates of morbidity and mortality, but no effective treatments. The lack of effective treatments and unacceptably high mortality rates for ARDS are partly due to an incomplete understanding of the mechanisms that control ALI/ARDS and subsequent vascular repair. Transforming growth factors (TGFs) are a class of growth factors that regulate the vascular response to inflammation, including migration, proliferation, and differentiation of cells comprising the lung vasculature. Here we review studies that describe the impact of the TGF family on inflammatory lung injury and subsequent vascular repair and fibrosis. We highlight gaps in understanding TGF isoform-specific roles in ALI/ARDS and outline directions for future research in the field of TGF-dependent regulation of inflammatory lung injury and vascular repair. Functional roles of the TGFs have been investigated in ALI/ARDS pathogenesis and pulmonary fibrosis, with a predominance for studies showing a proinjurious and profibrotic impact of TGF-β1. Studies have also shown that TGF-α is positively associated with inflammatory lung injury and fibrosis. However, the contributions of TGF-β2 and TGF-β3 to ALI/ARDS are unclear, and the contributions of all the TGF isoforms to vascular repair after ALI/ARDS are not well characterized. Improved understanding of the regulation of inflammatory lung injury and repair by the TGFs could lead to the development of a safe and effective treatment strategy for patients with ALI/ARDS.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L539-L554"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12539375/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scar wars: the viral menace.","authors":"Sara Kass-Gergi, Nicolas P Holcomb, Michael M Maiden, Laurence C Eisenlohr, Andrew E Vaughan","doi":"10.1152/ajplung.00189.2025","DOIUrl":"10.1152/ajplung.00189.2025","url":null,"abstract":"<p><p>Pulmonary fibrosis (PF) is a severe consequence of respiratory infections, characterized by excessive extracellular matrix deposition and irreversible lung architectural damage. Once considered a rare condition, PF is now increasingly recognized in the wake of viral infections, particularly among survivors of viral-induced acute respiratory distress syndrome (ARDS). The COVID-19 pandemic has highlighted in bold relief the observation that many survivors of severe viral pneumonia do not recover fully but develop chronic fibrotic changes that impair lung function. This review examines the clinical evidence and underlying mechanisms linking viral infections-COVID-19, influenza, and other respiratory viruses-to the onset of pulmonary fibrosis. By probing the mechanisms of cellular injury, immune dysregulation, and aberrant repair mechanisms, we aim to illuminate the pathways that transform an acute viral insult into a chronic, fibrotic disease.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L555-L569"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145123879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computer model-based injury prediction and evaluation of lung function in mice with acute and ventilator-induced lung injuries.","authors":"Elizabeth Kaye, Alexander Sosa, Katharine D Warner, David J Albers, Peter D Sottile, Bradford J Smith","doi":"10.1152/ajplung.00248.2025","DOIUrl":"10.1152/ajplung.00248.2025","url":null,"abstract":"<p><p>Invasive mechanical ventilation is a lifesaving intervention for patients with acute respiratory distress syndrome (ARDS) but it also causes ventilator-induced lung injury (VILI) that can be challenging to avoid due to interpatient and temporal heterogeneity. Thus, the aim of this study was to characterize and predict experimental VILI using readily available measures of lung function. Initially healthy (CTL) and hydrochloric acid (HCL) lung-injured mice were ventilated for 4 h at positive end-expiratory pressure (PEEP) 1, 3, or 8 cmH₂O to produce graded VILI severity as measured in lung function, alveolocapillary leak, and inflammation. Optimally protective PEEP was found to be 8 and 3 cmH₂O in the HCL and CTL groups, respectively. A novel computational model was fit to the data to investigate elastance dynamics described by the \"compliance factor\" (C_F), which was also used to predict VILI over 4 subsequent hours of ventilation. The model C_F is a sensitive measure of injury-induced alterations in the pressure and pressure history dependence of lung elastance that are known to correlate with recruitment and derecruitment dynamics. The C_F was then combined with PEEP and plateau pressures calculated from 10 min at the start of prolonged ventilation and used to accurately predict VILI outcomes measured 4 h later. This model outperformed other commonly used measures of injury such as driving pressure and mechanical power. The computer model provides a new tool for understanding lung dynamics and for predicting VILI. In future work, this approach could be used to guide identification of lung-protective ventilation settings.<b>NEW & NOTEWORTHY</b> Computer model-based analysis of lung function in healthy and lung-injured mice showed that model compliance factor (C_F) characteristics were sensitive measures of acute lung injury and ventilator-induced lung injury (VILI) severity. The [Formula: see text] Area, calculated from C_F and pressures from <i>minutes 5-15</i> of ventilation, was a stronger predictor of VILI measured 4 h later than the driving pressure or mechanical power, suggesting potential utility for monitoring ventilation safety and guiding ventilator adjustments to reduce VILI.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L598-L611"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145181819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sorted-cell proteomics reveals an AT1-associated epithelial cornification phenotype and suggests endothelial redox imbalance in human bronchopulmonary dysplasia.","authors":"Mereena George Ushakumary, William B Chrisler, Gautam Bandyopadhyay, Heidie Huyck, Brittney L Gorman, Naina Beishembieva, Ariana Pitonzo, Zhenli J Lai, Thomas L Fillmore, Isaac Kwame Attah, Gail Deutsch, Jeffrey M Purkerson, Andrew M Dylag, Ravi S Misra, James P Carson, Joshua N Adkins, Gloria S Pryhuber, Geremy C Clair","doi":"10.1152/ajplung.00098.2025","DOIUrl":"10.1152/ajplung.00098.2025","url":null,"abstract":"<p><p>Bronchopulmonary dysplasia (BPD) is a neonatal lung disease characterized by inflammation and scarring leading to long-term tissue damage. Previous whole tissue proteomics identified BPD-specific proteome changes and cell type shifts. Little is known about the proteome-level changes within specific cell populations in disease. Here, we sorted epithelial (EPI) and endothelial (ENDO) cell populations based on their differential surface markers from normal and BPD human lungs. Using a low-input compatible sample preparation method (MicroPOT), proteins were extracted and digested into peptides and subjected to liquid chromatography-tandem mass spectrometry (LC-MS/MS) proteome analysis. Of the 4,970 proteins detected, 293 were modulated in abundance or detection in the EPI population and 422 were modulated in ENDO cells. Modulation of proteins associated with actin-cytoskeletal function, such as SCEL, LMO7, and TBA1B was observed in the BPD EPIs. Using confocal imaging and analysis, we validated the presence of aberrant multilayer-like structures comprising SCEL and LMO7, known to be associated with epidermal cornification, in the human BPD lung. This is the first report of the accumulation of cornification-associated proteins in BPD. Their localization in the alveolar parenchyma, primarily associated with alveolar type 1 (AT1) cells, suggests a role in the BPD postinjury response. In the ENDOs, redox balance and mitochondrial function pathways were modulated. Alternative mRNA splicing and cell proliferative functions were elevated in both populations, suggesting potential dysregulation of cell progenitor fate. This study characterized the proteome of epithelial and endothelial cells from the BPD lung for the first time, identifying population-specific changes in BPD pathogenesis.<b>NEW & NOTEWORTHY</b> The study is the first to perform proteomics on sorted pulmonary epithelial and endothelial populations from bronchopulmonary dysplasia (BPD) and age-matched control human donors. We identified an increase in cornification-associated proteins in BPD (e.g., SCEL and LMO7), and evidenced the presence of multilayered structures unique to BPD alveolar regions, associated with alveolar type 1 (AT1) cells. By changing the nature and/or biomechanical properties of the epithelium, these structures may alter the behavior of other alveolar cell types potentially contributing to the arrested alveolarization observed in BPD. Finally, our data suggest the modulation of cell proliferation and redox homeostasis in BPD providing potential mechanisms for the reduced vascular growth associated with BPD.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L570-L582"},"PeriodicalIF":3.5,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145079523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial cell interactions with immune cells and fibroblasts in the pulmonary microenvironment: From the developing to the aging lung Sientific Session III ReSPIRE 2025.","authors":"Nunzia Caporarello, Dolly Mehta, Yoshikazu Tsukasaki, Anasuya Sarkar, Benjamin Colby Crawford, Natalie N Bauer","doi":"10.1152/ajplung.00311.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00311.2025","url":null,"abstract":"<p><p>Session III of the inaugural biennial Research Symposium on Pulmonary Injury and Repair of the Endothelium (ReSPIRE) highlighted key advancements in endothelial-inflammatory cell interactions. The work presented illustrates a growing recognition that pulmonary endothelial cell interactions and direct cross-talk with inflammatory cells are integral in both health and disease in the developing and aging lung. Data presented detail the impact of targeting neutrophil- and macrophage-endothelial interactions in acute lung injury, and the role of fibroblast-endothelial inflammatory communication in interstitial pulmonary fibrosis of the aging lung. In the developing lung the paradoxical responses of the pulmonary circulation to inflammatory cell interactions and mediators illustrate the complexities in cross-talk. State-of-the-art advances in intravital microscopy have recently revealed our ability to visualize and measure the mechanotransduction involved in neutrophil migration. This review highlights these recent advances and suggests future directions for understanding pulmonary endothelial-inflammatory cell cross-talk.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145306683","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Are alveolar type 2 cells \"oversaturated\" in obesity and ARDS?","authors":"Avnee Jaya Kumar, Mark L Hepokoski","doi":"10.1152/ajplung.00325.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00325.2025","url":null,"abstract":"","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145290610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Roles of Peripheral and Central µ₁-Opioid Receptors in the Fentanyl-Induced Cardiorespiratory Responses.","authors":"Jianguo Zhuang, Xiuping Gao, Zikuan Chen, Shan Shi, Fadi Xu","doi":"10.1152/ajplung.00278.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00278.2025","url":null,"abstract":"<p><p><b>Background:</b> Intravenous bolus (IVb) injection of fentanyl triggers a vagal-mediated immediate apnea and subsequent respiratory depression in anesthetized rats. This study compared the gender-dependence of these responses in conscious rats and roles of peripheral and central opioid receptors (ORs), especially μ- and μ1-ORs in the genesis of these responses. <b>Methods:</b> Cardiorespiratory responses to IVb injection of fentanyl (50 μg kg_-1) were recorded in male and female conscious rats (<i>Study I</i>). The same protocols were performed after: naloxone (NLX) and naloxone methiodide (NLM) to systemically and peripherally antagonize ORs respectively (<i>Study II</i>); CTAP and methylnaltrexone (MNTX) to systemically and peripherally block μ-ORs (<i>Study III</i>); and naloxonazine (NLZ) to systemically block μ₁-ORs (<i>Study IV</i>). <b>Results:</b> IVb injection of fentanyl induced an immediate life-threatening apnea (~1.5 min) and severe bradycardia, which was followed by cardiorespiratory depression lasting for ~55 min with little difference between genders. NLX fully eliminated and CTAP substantially blunted all cardiorespiratory responses to fentanyl, while NLM and MNTX substantially minimized the immediate apnea and reduced bradycardia by ~50% with limited impact on the subsequent cardiorespiratory depression. NLZ nearly abolished the fentanyl-evoked responses. <b>Conclusion:</b> Our results indicate that peripherally restricted OR (particularly μ₁-OR) antagonism prevents the fentanyl-induced immediate apnea, but fails to change the subsequent respiratory depression.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145290656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adrenomedullin Overexpression Protects Mice from Experimental Bronchopulmonary Dysplasia and Associated Pulmonary Hypertension.","authors":"Shyam Thapa, Poonam Sarkar, M Waleed Gaber, Roberto Barrios, Madhulata Chauhan, Chandrasekhar Yallampalli, Binoy Shivanna","doi":"10.1152/ajplung.00234.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00234.2025","url":null,"abstract":"<p><p>Bronchopulmonary dysplasia (BPD) associated pulmonary hypertension (PH) or BPD-PH is a lung disease of infants with significant morbidity. Adrenomedullin (Adm) is an angiogenic peptide that signals through calcitonin receptor-like receptor (Calcrl) and receptor activity modifying protein 2 (RAMP2). <i>Adm</i> deficiency potentiates hyperoxia-induced experimental BPD-PH in mice; however, whether <i>Adm</i> overexpression can mitigate this lung disease is unclear. Thus, we tested the hypothesis that <i>Adm</i> overexpression attenuates hyperoxia (HO)-induced murine experimental BPD-PH by using a novel transgenic mouse that overexpresses <i>Adm</i> globally (<i>Adm^hi/hi</i> mice). One-day-old <i>Adm^hi/hi</i> mice or their wild-type littermates (<i>Adm^+/+</i> mice) were exposed to HO (FiO₂ 70%) for 14 d and allowed to recover in normoxia (NO, FiO₂ 21%) for an additional 14 d. Controls were maintained in NO for 28 d. On postnatal day (P) 14, we harvested the lungs to determine the extent of <i>Adm</i> expression and apoptosis. On P28, we quantified alveolarization, lung vascularization, and PH. HO-exposed <i>Adm^+/+</i> mice demonstrated increased lung apoptosis, decreased alveolarization and lung vascularization, and indices of PH, indicating that neonatal HO exposure causes BPD-PH. However, <i>Adm</i> overexpression attenuated experimental BPD-PH, as evident by the decreased extent of hyperoxia-induced lung apoptosis and inflammation, alveolar and vascular simplification, pulmonary vascular remodeling, and PH in <i>Adm^hi/hi</i> mice than in <i>Adm^+/+</i> mice. Collectively, our results demonstrate that <i>Adm</i> overexpression attenuates HO-induced murine experimental BPD-PH, emphasizing the therapeutic potential of Adm for BPD-PH in preterm infants.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From Development to Regeneration: The Endothelial Interface in Lung Injury and Repair.","authors":"Lisandra Vila Ellis, David N Cornfield, Michael P Croglio, Mohammad N Islam, Jamie E Meegan","doi":"10.1152/ajplung.00236.2025","DOIUrl":"https://doi.org/10.1152/ajplung.00236.2025","url":null,"abstract":"<p><p>The pulmonary alveolar-capillary niche is a highly specialized interface that balances gas exchange with maintenance functions and repair. Advances in single cell transcriptomics have uncovered endothelial heterogeneity which underlies developmental angiogenesis and plastic responses to injury. Emerging evidence from a neonatal hyperoxia model highlights CAP1 to CAP2 transitions and the role of p53 in maintaining lineage fidelity. Beyond intrinsic lineage plasticity, circulating mediators such as cell-free hemoglobin drive endothelial barrier disruption through oxidative injury and lipid modification. As new signaling pathways and therapeutics targets emerge, complementary strategies are being developed at the cellular level, including adoptive transfer of mesenchymal stromal and immune cells, although mechanisms of endothelial adhesion and homing remain incompletely defined. Finally, biomechanical forces such as shear stress have become critical contextual cues for endothelial signaling, yet remain underrepresented in some experimental models. Together, these insights underscore the central role of endothelial heterogeneity, injury responses, and environmental cues in shaping pulmonary vascular health and repair, with implications for designing targeted therapies in both pediatric and adult lung disease.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145273557","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}