Respiratory Physiology & Neurobiology最新文献

{"title":"Danshensu methyl ester attenuated LPS-induced acute lung injury by inhibiting TLR4/NF-κB pathway","authors":"Xuejia Han ,&nbsp;Wensi Ding ,&nbsp;Guiwu Qu ,&nbsp;Youjie Li ,&nbsp;Pingyu Wang ,&nbsp;Jiahui Yu ,&nbsp;Mingyue Liu ,&nbsp;Xiulan Chen ,&nbsp;Shuyang Xie ,&nbsp;Jiankai Feng ,&nbsp;Sen Xu","doi":"10.1016/j.resp.2024.104219","DOIUrl":"10.1016/j.resp.2024.104219","url":null,"abstract":"<div><p><span><span>Acute Lung Injury (ALI) manifests as an acute exacerbation of pulmonary inflammation with high mortality. The potential application of </span>Danshensu<span><span><span><span> methyl ester (DME, synthesized in our lab) in ameliorating ALI has not been elucidated. Our results demonstrated that DME led to a remarkable reduction in lung injury. DME promoted a marked increase in </span>antioxidant enzymes, like </span>superoxide dismutase<span> (SOD), and glutathione<span> (GSH), accompanied by a substantial decrease in reactive oxygen species<span> (ROS), myeloperoxidase (MPO), and </span></span></span></span>malondialdehyde (MDA). Moreover, DME decreased the production of IL-1β, TNF-α and IL-6, </span></span><em>in vitro</em> and <em>in vivo</em><span>. TLR4<span> and MyD88 expression is reduced in the DME-treated cells or tissues, which further leading to a decrease of p-p65 and p-IκBα. Meanwhile, DME effectively facilitated an elevation in cytoplasmic p65 expression. In summary, DME could ameliorate ALI by its antioxidant functionality and anti-inflammation effects through TLR4/NF-κB, which implied that DME may be a viable medicine for lung injury.</span></span></p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139500405","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Longitudinal changes in respiratory reactance in patients with COPD: associations with longitudinal change in air-trapping, exacerbations, and mortality","authors":"Yi Zhang ,&nbsp;Naoya Tanabe ,&nbsp;Susumu Sato ,&nbsp;Yusuke Shiraishi ,&nbsp;Tomoki Maetani ,&nbsp;Ryo Sakamoto ,&nbsp;Atsuyasu Sato ,&nbsp;Shigeo Muro ,&nbsp;Toyohiro Hirai","doi":"10.1016/j.resp.2024.104216","DOIUrl":"10.1016/j.resp.2024.104216","url":null,"abstract":"<div><h3>Introduction</h3><p><span>Air-trapping affects clinical outcomes in patients<span> with chronic obstructive pulmonary disease (COPD) and may be detected by reactance at 5 Hz (X5) on respiratory </span></span>oscillometry because X5 sensitively reflects the elasticity of the chest wall, airway and lung. However, the longitudinal association between X5 and air-trapping remains to be explored. This study aimed to test whether longitudinal changes in X5 could be associated with air-trapping progression, exacerbations, and mortality in patients with COPD.</p></div><div><h3>Methods</h3><p>In this prospective COPD observational study, the follow-up period consisted of the first 4 years to obtain longitudinal changes in X5 and residual volume (RV) and number of exacerbations and the remaining years (year 4 to 10) to test mortality. Patients were divided into large, middle, and small X5 decline groups based on the tertiles of longitudinal change in X5, and mortality after 4 years was compared between the groups.</p></div><div><h3>Results</h3><p><span>Patients with COPD (n = 114) were enrolled. The large X5 decline group (n = 38) showed a greater longitudinal change in RV and more exacerbations compared with the small X5 decline group (n = 39) in multivariable models adjusted for age, sex, body mass index, and smoking history. Long-term mortality after the 4-year follow-up was higher in the large X5 decline group than in the small X5 decline group (hazard ratio [95 % confidence interval] = 8.37[1.01, 69.0]) in the multivariable Cox </span>proportional hazard model.</p></div><div><h3>Conclusion</h3><p>Longitudinal changes in respiratory reactance could be associated with progressive air-trapping, exacerbation frequency, and increased mortality in patients with COPD.</p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139492004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss-of-function of chemoreceptor neurons in the retrotrapezoid nucleus: What have we learned from it?","authors":"George M.P.R. Souza,&nbsp;Stephen B.G. Abbott","doi":"10.1016/j.resp.2024.104217","DOIUrl":"10.1016/j.resp.2024.104217","url":null,"abstract":"<div><p><span>Central respiratory chemoreceptors<span> are cells in the brain that regulate breathing in relation to arterial pH and PCO</span></span>₂<span><span><span>. Neurons located at the retrotrapezoid nucleus (RTN) have been hypothesized to be central chemoreceptors and/or to be part of the </span>neural network<span> that drives the central respiratory chemoreflex. The inhibition or ablation of RTN chemoreceptor neurons has offered important insights into the role of these cells on central respiratory chemoreception and the neural </span></span>control of breathing<span> over almost 60 years since the original identification of acid-sensitive properties of this ventral medullary site. Here, we discuss the current definition of chemoreceptor neurons in the RTN and describe how this definition has evolved over time. We then summarize the results of studies that use loss-of-function approaches to evaluate the effects of disrupting the function of RTN neurons on respiration. These studies offer evidence that RTN neurons are indispensable for the central respiratory chemoreflex in mammals and exert a tonic drive to breathe at rest. Moreover, RTN has an interdependent relationship with oxygen sensing mechanisms for the maintenance of the neural drive to breathe and blood gas homeostasis. Collectively, RTN neurons are a genetically-defined group of putative central respiratory chemoreceptors that generate CO</span></span>₂-dependent drive that supports eupneic breathing and stimulates the hypercapnic ventilatory reflex.</p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139492006","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Axonal projection of the medullary expiratory neurons in the feline thoracic spinal cord","authors":"Kenta Kawamura ,&nbsp;Kazumasa Sasaki ,&nbsp;Sei-Ichi Sasaki ,&nbsp;Kazuhide Tomita","doi":"10.1016/j.resp.2024.104218","DOIUrl":"10.1016/j.resp.2024.104218","url":null,"abstract":"<div><p><span><span>Expiratory neurons in the caudal ventral respiratory group extend descending axons to the lumbar and sacral spinal cord, and they possess axon collaterals, the distribution of which has been well-documented. Likewise, these expiratory neurons extend axons to the </span>thoracic spinal cord and innervate thoracic expiratory </span>motoneurons<span><span>. These axons also give rise to collaterals, and their distribution may influence the strength of synaptic connectivity between the axons and the thoracic expiratory motoneurons. We investigated the distribution of axon collaterals in the thoracic spinal cord using a microstimulation<span> technique. This study was performed on cats; one cat was used to make an anatomical atlas and six were used in the experiment. Extracellular spikes of expiratory neurons were recorded in artificially ventilated cats. The thoracic spinal gray matter was microstimulated from dorsal to ventral sites at 100-μm intervals using a glass-insulated tungsten microelectrode<span> with a current of 150–250 μA. The stimulation tracks were made at 1 mm intervals along the spinal cord in segments Th9 to Th13, and the effective stimulating sites of antidromic activation in axon collaterals were systematically mapped. The effective stimulating sites in the </span></span></span>contralateral<span> thoracic spinal cord with expiratory neurons in the caudal ventral respiratory group (cVRG) occupied 14.4% of the total length of the thoracic spinal cord examined. The mean percentage of effective stimulating tracks per unit was 18.6 ± 4.4%. The distribution of axon collaterals of expiratory neurons in the feline thoracic spinal cord indeed resembled that reported in the upper lumbar spinal cord. We propose that a single medullary expiratory neuron exerts excitatory effects across multiple segments of the thoracic spinal cord via its collaterals.</span></span></p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139474686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neural oscillations underlying the neural gating of respiratory sensations in generalized anxiety disorder","authors":"Kai-Jie Liang ,&nbsp;Chia-Hsiung Cheng ,&nbsp;Chia-Yih Liu ,&nbsp;Shih-Chieh Hsu ,&nbsp;Andreas von Leupoldt ,&nbsp;Valentina Jelinčić ,&nbsp;Pei-Ying S. Chan","doi":"10.1016/j.resp.2024.104215","DOIUrl":"10.1016/j.resp.2024.104215","url":null,"abstract":"<div><p><span>Individuals with generalized anxiety disorder (GAD) have been shown to have altered neural gating of respiratory sensations (NGRS) using respiratory-related </span>evoked potentials<span> (RREP); however, corresponding neural oscillatory activities remain unexplored. The present study aimed to investigate altered NGRS in individuals with GAD using both time and time-frequency analysis. Nineteen individuals with GAD and 28 healthy controls were recruited. Paired inspiratory occlusions were delivered to elicit cortical neural activations measured from electroencephalography. The GAD group showed smaller N1 amplitudes to the first stimulus (S1), lower evoked gamma and larger evoked beta oscillations compared to controls. Both groups showed larger N1, P3, beta power and theta power in response to S1 compared to S2, suggesting a neural gating phenomenon. These findings suggest that N1, gamma and beta frequency oscillations may be indicators for altered respiratory sensation in GAD populations and that the N1, P3, beta and theta oscillations can reflect the neural gating of respiratory sensations.</span></p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139420820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Respiratory sinus arrhythmia in spontaneously breathing, unanesthetized newborn and adult Wistar rats","authors":"Nana Sato Hashizume,&nbsp;Yoichiro Kitajima,&nbsp;Ryoji Ide,&nbsp;Eishi Nakamura,&nbsp;Chikako Saiki","doi":"10.1016/j.resp.2023.104207","DOIUrl":"10.1016/j.resp.2023.104207","url":null,"abstract":"<div><p>We examined respiratory sinus arrhythmia (RSA) and possible interaction with respiratory frequency (<em>f</em>_R) and heart rate (HR) in spontaneously breathing, unanesthetized newborn Wistar rats (2- to 5-day-old; n = 54) and the adult rats (8-week-old; n = 34). Instantaneous heart rate (<em>inst</em>-HR) was calculated as the reciprocal of the inter-beat-interval. For each breath, RSA was determined as the difference between the maximum and minimum <em>inst</em>-HR value. The absolute RSA or RSA% (RSA per HR) were calculated as the average RSA of 10 consecutive breaths. RSA (or RSA%) in the newborn rats was significantly lower than that in the adult rats. Correlation coefficient between RSA (or RSA%) and 1/<em>f</em>_R or HR/<em>f</em>_R, but not HR, was significant in newborn rats, whereas only that between RSA (or RSA%) and HR was significant in adult rats. The power spectrum density of heartbeat fluctuation was detectable in both age groups. The present findings suggest that RSA exists and could be influenced by <em>f</em>_R, rather than HR, in newborn rats.</p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S1569904823001957/pdfft?md5=be5f9721538f1393cb872c340643dbba&pid=1-s2.0-S1569904823001957-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139069064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Divergent expiratory braking activity of costal and crural diaphragm","authors":"Giovanni Tagliabue ,&nbsp;Michael Ji ,&nbsp;Danny J. Zuege ,&nbsp;Paul A. Easton","doi":"10.1016/j.resp.2023.104205","DOIUrl":"10.1016/j.resp.2023.104205","url":null,"abstract":"<div><h3>Background</h3><p>There is increasing clinical interest in understanding the contribution of the diaphragm in early expiration, especially during mechanical ventilation. However, current experimental evidence is limited, so essential activity of the diaphragm during expiration and diaphragm segmental differences in expiratory activity, are unknown.</p></div><div><h3>Objectives</h3><p>To determine if: 1) the diaphragm is normally active into expiration during spontaneous breathing and hypercapnic ventilation, 2) expiratory diaphragmatic activity is distributed equally among the segments of the diaphragm, costal and crural.</p></div><div><h3>Methods</h3><p>In 30 spontaneously breathing male and female canines, awake without confounding anesthetic, we measured directly both inspiratory and expiratory electrical activity (EMG), and corresponding mechanical shortening, of costal and crural diaphragm, during room air and hypercapnia.</p></div><div><h3>Results</h3><p>During eupnea, costal and crural diaphragm are active into expiration, showing significant and distinct expiratory activity, with crural expiratory activity greater than costal, for both magnitude and duration. This diaphragm segmental difference diverged further during progressive hypercapnic ventilation: crural expiratory activity progressively increased, while costal expiratory activity disappeared.</p></div><div><h3>Conclusion</h3><p>The diaphragm is not passive during expiration. During spontaneous breathing, expiratory activity -“braking”- of the diaphragm is expressed routinely, but is not equally distributed. Crural muscle “braking” is greater than costal muscle in magnitude and duration.</p><p>With increasing ventilation during hypercapnia, expiratory activity -“braking”- diverges notably. Crural expiratory activity greatly increases, while costal expiratory “braking” decreases in magnitude and duration, and disappears.</p><p>Thus, diaphragm expiratory \"braking\" action represents an inherent, physiological function of the diaphragm, distinct for each segment, expressing differing neural activation.</p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2023-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138885983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic intermittent hypoxia attenuates noradrenergic innervation of hypoglossal motor nucleus","authors":"Rachael Herlihy ,&nbsp;Leonardo Frasson Dos Reis ,&nbsp;Anzor Gvritishvili ,&nbsp;Maya Kvizhinadze ,&nbsp;Elizabeth Dybas ,&nbsp;Atul Malhotra ,&nbsp;Victor B. Fenik ,&nbsp;Irma Rukhadze","doi":"10.1016/j.resp.2023.104206","DOIUrl":"10.1016/j.resp.2023.104206","url":null,"abstract":"<div><p><span>The state-dependent noradrenergic activation of hypoglossal motoneurons<span> plays an important role in the maintenance of upper airway patency<span><span> and pathophysiology of </span>obstructive sleep apnea<span> (OSA). Chronic intermittent hypoxia (CIH), a major pathogenic factor of OSA, contributes to the risk for developing </span></span></span></span>neurodegenerative disorders<span><span> in OSA patients. Using anterograde tracer, channelrhodopsin-2, we mapped axonal projections from noradrenergic A7 and SubCoeruleus neurons to </span>hypoglossal nucleus<span> in DBH-cre mice and assessed the effect of CIH on these projections. We found that CIH significantly reduced the number of axonal projections from SubCoeruleus neurons to both dorsal (by 68%) and to ventral (by73%) subregions of the hypoglossal motor nucleus compared to sham-treated animals. The animals’ body weight was also negatively affected by CIH. Both effects, the decrease in axonal projections and body weight, were more pronounced in male than female mice, which was likely caused by less sensitivity of female mice to CIH as compared to males. The A7 neurons appeared to have limited projections to the hypoglossal nucleus. Our findings suggest that CIH-induced reduction of noradrenergic innervation of hypoglossal motoneurons may exacerbate progression of OSA, especially in men.</span></span></p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2023-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139025467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of the NLRP3 inflammasome on increased hypoxic ventilation response after CIH exposure in mice","authors":"Xinyun Jia ,&nbsp;Jianxia Sun ,&nbsp;Qingya Zhuo ,&nbsp;Baosheng Zhao ,&nbsp;Yuzhen Liu","doi":"10.1016/j.resp.2023.104204","DOIUrl":"10.1016/j.resp.2023.104204","url":null,"abstract":"<div><h3>Background</h3><p><span>Chronic intermittent hypoxia<span> (CIH) increases the hypoxic ventilation response (HVR). The downstream cytokine IL-1β of the NLRP3 inflammasome regulates respiration by acting on the </span></span>carotid body<span> (CB) and neurons in the respiratory center, but the effect of the NLRP3 inflammasome on HVR induced by CIH remains unclear.</span></p></div><div><h3>Objective</h3><p>To investigate the effect of NLRP3 on the increased HVR and spontaneous apnea events and duration induced by CIH, the expression and localization of NLRP3 in the respiratory regulatory center of the rostral ventrolateral medulla (RVLM), and the effect of CIH on the activation of the NLRP3 inflammasome in the RVLM.</p></div><div><h3>Methods</h3><p><span>Eighteen male, 7-week-old C57BL/6 N mice and eighteen male, 7-week-old C57BL/6 N NLRP3 knockout mice were randomly divided into CON-WT, CON-NLRP3</span>^-/-, CIH-WT and CIH-NLRP3^-/-<span><span> groups. Respiratory changes in mice were continuously detected using whole-body plethysmography. The expression and localization of the NLRP3 protein and the formation of apoptosis-associated speck-like protein containing CARD (ASC) specks were detected using immunofluorescence </span>staining.</span></p></div><div><h3>Results</h3><p><span>NLRP3 knockout reduced the increased HVR and the incidence and duration of spontaneous apnea events associated with CIH. The increase in HVR caused by CIH partially recovered after reoxygenation. After CIH, NLRP3 inflammasome activation in the RVLM, which is related to </span>respiratory regulation after hypoxia, increased, which was consistent with the trend of the ventilation response.</p></div><div><h3>Conclusion</h3><p>The NLRP3 inflammasome may be involved in the increase in the HVR and the incidence and duration of spontaneous apnea induced by CIH. NLRP3 inhibitors may help reduce the increase in the HVR after CIH, which is important for ensuring sleep quality at night in patients<span> with obstructive sleep apnea.</span></p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138745075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Paralemmin-3 augments lipopolysaccharide-induced acute lung injury with M1 macrophage polarization via the notch signaling pathway","authors":"Xuxin Chen ,&nbsp;Fan Wang ,&nbsp;Jian Tang ,&nbsp;Jiguang Meng,&nbsp;Zhihai Han","doi":"10.1016/j.resp.2023.104203","DOIUrl":"https://doi.org/10.1016/j.resp.2023.104203","url":null,"abstract":"<div><h3>Background</h3><p>Acute lung injury (ALI) involves severe lung damage and respiratory failure, which are accompanied by alveolar macrophage (AM) activation. The aim of this article is to verify the influence of paralemmin-3 (PALM3) on alveolar macrophage (AM) polarization in ALI and the underlying mechanism of action.</p></div><div><h3>Methods</h3><p>An ALI rat model was established by successive lipopolysaccharide (LPS) inhalations. The influence of PALM3 on the survival rate, severity of lung injury, and macrophage polarization was analyzed. Furthermore, we explored the underlying mechanism of PALM3 in regulating macrophage polarization.</p></div><div><h3>Results</h3><p>PALM3 overexpression increased mortality of ALI rats, augmented lung pathological damage, and promoted AM polarization toward M1 cells. Conversely, PALM3 knockdown had the opposite effects. Mechanistically, PALM3 might promote M1 polarization by acting as an adaptor to facilitate transduction of Notch signaling.</p></div><div><h3>Conclusion</h3><p>PALM3 aggravates lung injury and induces macrophage polarization toward M1 cells by activating the Notch signaling pathway in LPS-induced ALI, which may shed light on ALI/ARDS treatments.</p></div>","PeriodicalId":20961,"journal":{"name":"Respiratory Physiology & Neurobiology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2023-12-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S156990482300191X/pdfft?md5=116d5dd81d3a59b0c50605f74dbb0cea&pid=1-s2.0-S156990482300191X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138769764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}