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

{"title":"Inference of alveolar capillary network connectivity from blood flow dynamics.","authors":"Kerstin Schmid, Andy L Olivares, Oscar Camara, Wolfgang M Kuebler, Matthias Ochs, Andreas C Hocke, Sabine C Fischer","doi":"10.1152/ajplung.00025.2024","DOIUrl":"10.1152/ajplung.00025.2024","url":null,"abstract":"<p><p>The intricate lung structure is crucial for gas exchange within the alveolar region. Despite extensive research, questions remain about the connection between capillaries and the vascular tree. We propose a computational approach combining three-dimensional (3-D) morphological modeling with computational fluid dynamics simulations to explore alveolar capillary network connectivity based on blood flow dynamics. We developed three-dimensional sheet-flow models to accurately represent alveolar capillary morphology and conducted simulations to predict flow velocities and pressure distributions. Our approach leverages functional features to identify plausible system architectures. Given capillary flow velocities and arteriole-to-venule pressure drops, we deduced arteriole connectivity details. Preliminary analyses for nonhuman species indicate a single alveolus connects to at least two 20-µm arterioles or one 30-µm arteriole. Hence, our approach narrows down potential connectivity scenarios, but a unique solution may not always be expected. Integrating our blood flow model results into our previously published gas exchange application, Alvin, we linked these scenarios to gas exchange efficiency. We found that increased blood flow velocity correlates with higher gas exchange efficiency. Our study provides insights into pulmonary microvasculature structure by evaluating blood flow dynamics, offering a new strategy to explore the morphology-physiology relationship that is applicable to other tissues and organs. Future availability of experimental data will be crucial in validating and refining our computational models and hypotheses.<b>NEW & NOTEWORTHY</b> The alveolus is pivotal for gas exchange. Its complex, dynamic nature makes structural experimental studies challenging. Computational modeling offers an alternative. We developed a data-based three-dimensional (3-D) model of the alveolar capillary network and performed blood flow simulations within it. Choosing a novel perspective, we inferred structure from function. We systematically varied the properties of vessels connected to our capillary network and analyzed simulation results for blood flow and gas exchange to obtain plausible vessel configurations.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L852-L866"},"PeriodicalIF":3.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339332","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":"Moving on from clinical animal-derived surfactants to peptide-based synthetic pulmonary surfactant.","authors":"Frans J Walther, Alan J Waring","doi":"10.1152/ajplung.00186.2024","DOIUrl":"10.1152/ajplung.00186.2024","url":null,"abstract":"<p><p>Research on lung surfactant has exerted a great impact on newborn respiratory care and significantly improved survival and outcome of preterm infants with respiratory distress syndrome (RDS) due to surfactant deficiency because of lung immaturity. Current clinical, animal-derived, surfactants are among the most widely tested compounds in neonatology. However, limited availability, high production costs, and ethical concerns about using animal-derived products constitute important limitations in their universal application. Synthetic lung surfactant offers a promising alternative to animal-derived surfactants by providing improved consistency, quality and purity, availability and scalability, ease of production and lower costs, acceptance, and safety for the treatment of neonatal RDS and other lung conditions. Third-generation synthetic surfactants built around surfactant protein B (SP-B) and C (SP-C) peptide mimics stand at the forefront of innovation in neonatal pulmonary medicine, while nasal continuous positive airway pressure (nCPAP) has become the standard noninvasive respiratory support for preterm infants. nCPAP can prevent the risk of chronic lung disease (bronchopulmonary dysplasia) and reduce lung injury by avoiding intubation and mechanical ventilation, is a relatively simple technique, and can be initiated safely and effectively in the delivery room. Combining nCPAP with noninvasive, preferably aerosol, delivery of synthetic lung surfactant promises to improve respiratory outcomes for preterm infants, especially in low- and middle-income countries.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L883-L889"},"PeriodicalIF":3.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455992","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":"Eosinophils prevent diet-induced airway hyperresponsiveness in mice on a high-fat diet.","authors":"Becky J Proskocil, Gina N Bash, David B Jacoby, Allison D Fryer, Zhenying Nie","doi":"10.1152/ajplung.00213.2024","DOIUrl":"10.1152/ajplung.00213.2024","url":null,"abstract":"<p><p>Eosinophils contribute to metabolic homeostasis and airway hyperresponsiveness, but their specific role in obesity-related airway hyperresponsiveness remains unclear. To address this, we used transgenic mice that overexpress interleukin-5 (IL-5) in peripheral T cells (+IL-5T) and wild-type controls. On a normal diet, +IL-5T and wild-type mice have similar body weight, body fat, and airway nerve-mediated reflex bronchoconstriction in response to inhaled serotonin. Feeding wild-type mice a 61.6% high-fat diet resulted in significantly increased body weight, body fat, fasting glucose, fasting insulin, and reflex bronchoconstriction induced by serotonin, which was blocked by vagotomy. In contrast, +IL-5T mice on a high-fat diet gained less body weight and fat than wild-type mice on the same diet and did not exhibit potentiation in fasting glucose, fasting insulin, or reflex bronchoconstriction induced by serotonin. Compared with wild-type mice, +IL-5T mice on normal diet had significantly more adipose tissue eosinophils, and this was further increased by high-fat diet. High-fat diet did not increase adipose tissue eosinophils in wild-type mice. Our findings suggest that adipose tissue eosinophils may play a role in regulating body fat, thereby reducing insulin, which is a mediator of obesity-related airway hyperresponsiveness. Thus, our data indicate adipose tissue eosinophils may be an important avenue for research in obesity-related asthma.<b>NEW & NOTEWORTHY</b> This study investigates how eosinophils influence systemic metabolism and airway function in obesity. Known for their immune functions, eosinophils also mitigate obesity-related hyperinsulinemia, reducing airway hyperresponsiveness in obese mice models. The findings suggest potential therapeutic strategies targeting the intricate interplay among neurons, eosinophils, and the endocrine system to alleviate asthma in obesity. This research provides novel insights into the critical neuro-immune-endocrine interactions essential for managing obesity-related asthma.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L867-L875"},"PeriodicalIF":3.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339329","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":"Mechanisms of lung endothelial cell injury and survival in pulmonary arterial hypertension.","authors":"Ygor Marinho, Elizabeth S Villarreal, Omar Loya, Suellen D Oliveira","doi":"10.1152/ajplung.00208.2024","DOIUrl":"10.1152/ajplung.00208.2024","url":null,"abstract":"<p><p>Pulmonary arterial hypertension (PAH) is a progressive, chronic, and incurable inflammatory pulmonary vascular disease characterized by significant sex bias and largely unexplored microbial-associated molecular mechanisms that may influence its development and sex prevalence across various subgroups. PAH can be subclassified as idiopathic, heritable, or associated with conditions such as connective tissue diseases, congenital heart defects, liver disease, infections, and chronic exposure to drugs or toxins. During PAH progression, lung vascular endothelial cells (ECs) undergo dramatic morphofunctional transformations in response to acute and chronic inflammation. These transformations include the appearance and expansion of abnormal vascular cell phenotypes such as those derived from apoptosis-resistant cell growth and endothelial-to-mesenchymal transition (EndoMT). Compelling evidence indicates that these endothelial phenotypes seem to be triggered by chronic lung vascular injury and dysfunction, often characterized by reduced secretion of vasoactive molecules like nitric oxide (NO) and exacerbated response to vasoconstrictors such as Endothelin-1 (ET-1), both long-term known contributors of PAH pathogenesis. This review sheds light on the mechanisms of EC dysfunction, apoptosis, and EndoMT in PAH, aiming to unravel the intricate interactions between ECs, pathogens, and other cell types that drive the onset and progression of this devastating disease. Ultimately, we hope to provide an overview of the complex functions of lung vascular ECs in PAH, inspiring novel therapeutic strategies that target these dysfunctional cells to improve the treatment landscape for PAH, particularly in the face of current and emerging global pathogenic threats.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L972-L983"},"PeriodicalIF":3.6,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11684956/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142455991","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":"Senescence of lung mesenchymal stem cells of preterm infants by cyclic stretch and hyperoxia via p21.","authors":"Judith Behnke, Maurizio J Goetz, Lena Holzfurtner, Pauline Korte, Astrid Weiss, Tayyab Shahzad, Jochen Wilhelm, Ralph T Schermuly, Stefano Rivetti, Saverio Bellusci, Harald Ehrhardt","doi":"10.1152/ajplung.00355.2023","DOIUrl":"10.1152/ajplung.00355.2023","url":null,"abstract":"<p><p>Phenotype distortion of lung resident mesenchymal stem cells (MSC) in preterm infants is a hallmark event in the pathogenesis of bronchopulmonary dysplasia (BPD). Here, we evaluated the impact of cyclic mechanical stretch (CMS) and hyperoxia (HOX). The negative action of HOX on proliferation and cell death was more pronounced at 80% than at 40%. Although the impact of CMS alone was modest, CMS plus HOX displayed the strongest effect sizes. Exposure to CMS and/or HOX induced the downregulation of PDGFRα, and cellular senescence preceded by p21 accumulation. p21 interference interfered with cellular senescence and resulted in aggravated cell death, arguing for a prosurvival mechanism. HOX 40% and limited exposure to HOX 80% prevailed in a reversible phenotype with reuptake of proliferation, while prolonged exposure to HOX 80% resulted in definite MSC growth arrest. Our mechanistic data explain how HOX and CMS induce the effects on MSC phenotype disruption. The results are congruent with the clinical observation that preterm infants requiring supplemental oxygen plus mechanical ventilation are at particular risk for BPD. Although inhibiting p21 is not a feasible approach, limiting the duration and magnitude of the exposures is promising.<b>NEW & NOTEWORTHY</b> Rarefication of lung mesenchymal stem cells (MSC) due to exposure to cyclic mechanical stretch (CMS) during mechanical ventilation with oxygen-rich gas is a hallmark of bronchopulmonary dysplasia in preterm infants, but the pathomechanistic understanding is incomplete. Our studies identify a common signaling mechanism mediated by p21 accumulation, leading to cellular senescence and cell death, most pronounced during the combined exposure with in principle reversible phenotype change depending on strength and duration of exposures.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L694-L711"},"PeriodicalIF":4.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563592/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339339","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":"MAP2K1 dampens cigarette smoke-induced inflammation via suppression of type I interferon pathway activation.","authors":"Ke-Qin Gong, Jourdan E Brune, Xiaoyun Guo, Anne M Manicone","doi":"10.1152/ajplung.00080.2024","DOIUrl":"10.1152/ajplung.00080.2024","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD), comprised of chronic bronchitis and emphysema, is a leading cause of morbidity and mortality worldwide. Mitogen-activated protein 2 kinase (MAP2K) pathway activation is present in COPD lung tissue and a genetic polymorphism in <i>Map2k1</i> associates with FEV1 decline in COPD, suggesting it may contribute to disease pathogenesis. To test the functional contribution of <i>Map2k1</i> in cigarette smoke (CS)-induced lung inflammation, we used a short-term CS exposure model in mice deficient in myeloid <i>Map2k1</i> (<i>Lysm^Cre+Mek1^fl</i>) and wild-type mice (<i>Mek1^fl</i>). Mice deficient in myeloid <i>Map2k1</i> had enhanced CS-induced lung inflammation characterized by increased neutrophil recruitment, vascular leak, augmented expression of elastolytic matrix metalloproteinases, and increased type I interferon-stimulated gene expression. The augmented neutrophilic inflammatory response could be abrogated by IFNAR1 blockade. These findings indicate that myeloid <i>Map2k1</i> regulates the immune response to CS via inhibition of the type I interferon pathway. Overall, these results suggest that <i>Map2k1</i> is a critical determinant in modulating the severity of CS-induced lung inflammation and its expression is protective.<b>NEW & NOTEWORTHY</b> Activation of the mitogen-activated protein kinases (MAPK)-ERK1/2 pathway is present in COPD lung tissue compared with healthy lungs. Our study using mice deficient in myeloid <i>Map2k1</i> reveals that <i>Map2k1</i> is a critical determinant in modulating the severity of CS-induced lung inflammation via suppression of type I interferon responses, and its expression is protective.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L740-L748"},"PeriodicalIF":4.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339334","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":"The bronchoalveolar lavage dilution conundrum: an updated view on a long-standing problem.","authors":"Sarah Haeger, Camille M Moore, Shannon A McManus, Peter K Moore, William J Janssen, Kara J Mould","doi":"10.1152/ajplung.00054.2024","DOIUrl":"10.1152/ajplung.00054.2024","url":null,"abstract":"<p><p>Bronchoalveolar lavage (BAL) is used by researchers to study molecular interactions within healthy and diseased human lungs. However, the utility of BAL fluid measurements may be limited by difficulties accounting for dilution of the epithelial lining fluid (ELF) sampled and inconsistent collection techniques. The use of endogenous markers to estimate ELF dilution has been proposed as a potential method to normalize acellular molecule measurements in BAL fluid, but these markers are also imperfect and prone to inaccuracy. The focus of this report is to review factors that affect the interpretation of acellular molecule measurements in lung ELF and present original data comparing the performance of several BAL dilution markers during health and in a human endobronchial endotoxin challenge model of acute inflammation. Our findings suggest that incomplete ELF and lavage fluid mixing, flux of markers across the alveolar barrier, and lung inflammation are all possible factors that can affect marker performance. Accounting for these factors, we show that commonly used markers including urea, total protein, albumin, and immunoglobulin M are likely unreliable BAL dilution markers. In contrast, surfactant protein D appears to be less affected by these factors and may be a more accurate and biologically plausible marker to improve the reproducibility of acellular BAL component measurements across individuals during health and inflammatory states.<b>NEW & NOTEWORTHY</b> In this report, mathematical prediction models and real-world measurements are used to compare the performance of molecular markers of dilution in bronchoalveolar lavage fluid samples. Effects of acute inflammation within individual subjects are highlighted. These findings inform recommendations for normalizing measurements across bronchoalveolar lavage samples and highlight the need for additional markers to improve the rigor of translational studies utilizing bronchoalveolar lavage measurements.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L807-L813"},"PeriodicalIF":4.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11560068/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142387264","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":"New faces: introducing the newest Editorial Board Fellows of the <i>American Journal of Physiology-Lung Cellular and Molecular Physiology</i>.","authors":"Larissa A Shimoda, Cristina M Alvira, Julie A Bastarache, Rodney D Britt, Wolfgang M Kuebler, Thiago S Moreira, Eric P Schmidt","doi":"10.1152/ajplung.00304.2024","DOIUrl":"https://doi.org/10.1152/ajplung.00304.2024","url":null,"abstract":"","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":"327 5","pages":"L669-L671"},"PeriodicalIF":3.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142543113","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":"Mechanisms of mechanical stimulation in the development of respiratory system diseases.","authors":"Tian Xia, Ziyin Pan, Haoxin Wan, Yongsen Li, Guocai Mao, Jun Zhao, Fangbiao Zhang, Shu Pan","doi":"10.1152/ajplung.00122.2024","DOIUrl":"10.1152/ajplung.00122.2024","url":null,"abstract":"<p><p>During respiration, mechanical stress can initiate biological responses that impact the respiratory system. Mechanical stress plays a crucial role in the development of the respiratory system. However, pathological mechanical stress can impact the onset and progression of respiratory diseases by influencing the extracellular matrix and cell transduction processes. In this article, we explore the mechanisms by which mechanical forces communicate with and influence cells. We outline the basic knowledge of respiratory mechanics, elucidating the important role of mechanical stimulation in influencing respiratory system development and differentiation from a microscopic perspective. We also explore the potential mechanisms of mechanical transduction in the pathogenesis and development of respiratory diseases such as asthma, lung injury, pulmonary fibrosis, and lung cancer. Finally, we look forward to new research directions in cellular mechanotransduction, aiming to provide fresh insights for future therapeutic research on respiratory diseases.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L724-L739"},"PeriodicalIF":3.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142339336","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":"Longitudinal importance of the soluble receptor for advanced glycation end-products in nonintubated hospitalized patients with COVID-19 pneumonia.","authors":"Katherine D Wick, Lianne Siegel, Cathryn Oldmixon, Jens D Lundgren, B Taylor Thompson, Chayse Jones, Carolyn Leroux, Michael A Matthay","doi":"10.1152/ajplung.00350.2023","DOIUrl":"10.1152/ajplung.00350.2023","url":null,"abstract":"<p><p>The soluble receptor for advanced glycation end-products (sRAGE) is a marker of alveolar type I cell injury associated with outcomes in COVID-19 pneumonia. How plasma sRAGE changes over time and whether it remains associated with long-term clinical outcomes beyond a single measurement in COVID-19 have not been well studied. We studied two cohorts in randomized clinical trials of monoclonal antibody treatment for COVID-19 (bamlanivimab and tixagevimab/cilgavimab). We first studied the association between baseline plasma sRAGE and 90-day clinical outcomes, which had been previously demonstrated in the bamlanivimab cohort, among hospitalized patients with COVID-19 supported with high-flow nasal oxygen (HFNO) or noninvasive ventilation (NIV) in the tixagevimab/cilgavimab study. Next, we investigated the relationship between <i>day 3</i> sRAGE and 90-day outcomes and how plasma sRAGE changes over the first 3 days of hospitalization in both clinical trial cohorts. We found that plasma sRAGE in the highest quartile in the HFNO/NIV participants in the tixagevimab/cilgavimab trial was associated with a significantly lower rate of 90-day sustained recovery [recovery rate ratio = 0.31, 95% confidence interval (CI) = 0.14-0.71, <i>P</i> = 0.005] and with a significantly higher rate of 90-day mortality (hazard ratio = 2.49, 95% CI = 1.15-5.43, <i>P</i> = 0.021) compared with the lower three quartiles. <i>Day 3</i> plasma sRAGE in both clinical trial cohorts remained associated with 90-day clinical outcomes. The trajectory of sRAGE was not influenced by treatment assignment. Our results indicate that plasma sRAGE is a valuable prognostic marker in COVID-19 up to 3 days after initial hospital presentation.<b>NEW & NOTEWORTHY</b> The soluble receptor for advanced glycation end-products (sRAGE) is a marker of alveolar type I epithelial cell injury associated with clinical outcomes in acute respiratory distress syndrome and, more recently, in hospitalized subjects with COVID-19. How plasma sRAGE changes over time and whether plasma sRAGE remains associated with long-term clinical outcomes beyond a single baseline measurement in patients with COVID-19 have not been well studied.</p>","PeriodicalId":7593,"journal":{"name":"American journal of physiology. Lung cellular and molecular physiology","volume":" ","pages":"L607-L614"},"PeriodicalIF":4.3,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11563646/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141791680","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}