8 results match your criteria: "Center of Emergency and Critical Medicine in Jinshan Hospital of Fudan University[Affiliation]"

Exacerbation of pulmonary fibrosis following acute lung injury via activin-A production by recruited alveolar macrophages.

J Thorac Dis

November 2024

Shanghai Key Laboratory of Lung Inflammation and Injury, Department of Pulmonary Medicine, Zhongshan Hospital, Fudan University, Shanghai, China.

Background: Acute respiratory distress syndrome (ARDS) is a complicated pathological cascade process of excessive pulmonary inflammation and alveolar epithelial cell apoptosis that results in respiratory dysfunction and failure. Some cases of ARDS can result in a more severe state of pulmonary fibrosis, referred to as postinjury lung fibrosis. The mortality and incidence rate of ARDS are high, particularly when it leads to continuing alveolar and interstitial fibrosis, which requires urgent treatment and appropriate management.

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Galectin-3 inhibition ameliorates alveolar epithelial cell pyroptosis in phosgene-induced acute lung injury.

Int Immunopharmacol

May 2024

Center of Emergency and Critical Medicine in Jinshan Hospital of Fudan University, Shanghai 201508, China; Research Center for Chemical Injury, Emergency and Critical Medicine of Fudan University, Shanghai 201508, China; Key Laboratory of Chemical Injury, Emergency and Critical Medicine of Shanghai Municipal Health Commission, Shanghai 201508, China. Electronic address:

Article Synopsis
  • Phosgene, a toxic gas, can lead to serious lung injuries in cases of accidental exposure, and the biological mechanisms behind this injury are not well understood.
  • Recent research using single-cell RNA sequencing identified that the protein Galectin-3 (Gal3) was present at significantly higher levels in the lungs of mice affected by phosgene-induced acute lung injury (P-ALI).
  • Inhibiting Gal3 and removing specific immune cells (alveolar macrophages) reduced lung cell death and damage in experimental models, suggesting targeting Gal3 could improve treatment strategies for P-ALI.
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The cuproptosis-related gene glutaminase promotes alveolar macrophage copper ion accumulation in chronic obstructive pulmonary disease.

Int Immunopharmacol

March 2024

Department of Pulmonary and Critical Care Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, Shanghai 200032, China; Shanghai Engineering Research Center of Internet of Things for Respiratory Medicine, 180 Fenglin Road, Shanghai 200032, China; Shanghai Key Laboratory of Lung Inflammation and Injury, 180 Fenglin Road, Shanghai 200032, China; Hebei Academy of Integrated Traditional Chinese and Western Medicine, Shijiazhuang 050091, Hebei, China; Research Center for Chemical Injury, Emergency and Critical Medicine of Fudan University, Fudan University, Shanghai 200540, China; Center of Emergency and Critical Medicine in Jinshan Hospital of Fudan University, Fudan University, Shanghai 200540, China; Key Laboratory of Chemical Injury, Emergency and Critical Medicine of Shanghai Municipal Health Commission, Shanghai 200540, China. Electronic address:

Cuproptosis, a novel mode of cell death, is strongly associated with a variety of diseases. However, the contribution of cuproptosis to the onset or progression of chronic obstructive pulmonary disease (COPD), the third most common chronic cause of mortality, is not yet clear. To investigate the potential role of cuproptosis in COPD, raw datasets from multiple public clinical COPD databases (including RNA-seq, phenotype, and lung function data) were used.

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Keratin 15 protects against cigarette smoke-induced epithelial mesenchymal transformation by MMP-9.

Respir Res

November 2023

Department of Pulmonary and Critical Care Medicine, Shanghai Respiratory Research Institute, Zhongshan Hospital, Fudan University, 180 Fenglin Rd, Shanghai, 200032, China.

Background: Chronic obstructive pulmonary disease (COPD), a chronic inflammatory lung disease, is a leading cause of morbidity and mortality worldwide. Prolonged cigarette smoking (CS) that causes irreversible airway remodeling and significantly reduces lung function is a major risk factor for COPD. Keratin15 (Krt15) cells with the potential of self-renewal and differentiation properties have been implicated in the maintenance, proliferation, and differentiation of airway basal cells; however, the role of Krt15 in COPD is not clear.

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LHQK is a patented Traditional Chinese Medicine (TCM) which is clinically used for acute tracheobronchitis, cough, and other respiratory diseases. Recent studies have proved that LHQK exhibits excellent clinical efficacy in the treatment of acute lung injury (ALI). However, the corresponding mechanisms remain largely unexplored.

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Alveolar epithelial cells (AECs) play a role in chemically induced acute lung injury (CALI). However, the mechanisms that induce alveolar epithelial type 2 cells (AEC2s) to proliferate, exit the cell cycle, and transdifferentiate into alveolar epithelial type 1 cells (AEC1s) are unclear. Here, we investigated the epithelial cell types and states in a phosgene-induced CALI rat model.

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Qingke Pingchuan granules (QKPCG), a patented traditional Chinese medicine, clinically, are recommended for acute tracheobronchitis, cough, community-acquired pneumonia, and other respiratory diseases. However, its potential protective effect and mechanism of action in acute lung injury (ALI) have not been explored. We aimed to explore the mechanisms underlying the protective role of QKPCG in ALI.

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Acute respiratory distress syndrome (ARDS) presents as a form of acute respiratory failure resulting from non-cardiogenic pulmonary edema due to excessive alveolocapillary permeability, which may be pulmonary or systemic in origin. In the last 3 years, the coronavirus disease 2019 pandemic has resulted in an increase in ARDS cases and highlighted the challenges associated with this syndrome, as well as the unacceptably high mortality rates and lack of effective treatments. Currently, clinical treatment remains primarily supportive, including mechanical ventilation and drug-based therapy.

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