Danhong injection alleviates sepsis-induced acute lung injury by regulating AGE/RAGE/AKT pathway.

SIRT6 inhibits intermittent hypoxia-induced lung injury by stabilizing NRF2.

Therapeutic targeting of oxidative-inflammatory crosstalk by Apelin-12 in neonatal hyperoxia-induced lung injury.

In 2019, a number of patients were hospitalized after the use of electronic cigarettes and displayed acute lung injuries. Such injury was categorized as e-cigarette or vaping associated lung injury (EVALI). Among these patients, Vitamin E acetate (VEA) was detected in most used electronic cigarette cartridges as well as the patients' bronchoalveolar lavage fluid, suggesting VEA to be a culprit of causing lung injury. Although further experiments verified the potential of VEA aerosol to cause cytotoxicity and lung injury, mechanisms of VEA aerosol toxicity are not well understood. In this study, we tested the toxicity of VEA, and its aerosol using a human macrophage model. VEA aerosols significantly induced oxidative stress as well as proinflammatory responses. In addition, the aerosol activated the aryl hydrocarbon receptor (AhR) signaling pathway, inducing CYP1A1 expression in human U937 monocyte-derived macrophages. Additionally, non-aerosolized VEA and VEA aerosol induce the expression of inflammatory markers such as interleukin (IL)-8 and cyclooxygenase (COX)-2 in an AhR-dependent manner as shown in CRISPR-cas9 AhR-knockout U937-derived human macrophages. These results suggest that VEA is an agonist for AhR and provide new potential mechanisms for lung injury induced by VEA aerosol inhalation via AhR activation in addition to the generation of oxidative stress.

Necroptosis mediated by FKBP5 in alveolar fibroblasts drives Pseudomonas aeruginosa-induced acute lung injury.

Ferrostatin-1 attenuates sepsis-induced lung injury by inhibiting ferroptosis via activation of the SLC7A11/GSH/GPX4 signaling pathway.

PKM2 from hyperactive neuron aggravate lung injury post-stroke by promoting FOXO3A/TXNIP mitochondria translocation in mice.

Therapeutic potential of Dahuang Mudan Decoction for severe acute pancreatitis: targeting oxidative stress and MAPK pathways through network pharmacology and experimental verification1.

Adenovirus induces pediatric pneumonia via triggering macrophage polarization and IL-6 production via NF-κB activation.

HO-1/Nrf2 activation orchestrates protection in sepsis-induced lung injury by suppressing CCR2hi monocyte recruitment and MAPK-driven inflammation.

Design and optimization of N-(3-((4-(1H-indol-3-yl)pyrimidin-2-yl)amino)phenyl)amide derivatives as potent anti-inflammatory agents against LPS-induced acute lung injury.

Ionizing radiation promotes lung injury by inducing ferroptosis-driven senescence in epithelial cells via NCOA4-mediated ferritinophagy.

Acute Respiratory Distress Syndrome (ARDS) remains a major cause of morbidity and mortality in trauma patients, rising from a complex interplay of direct lung injury, systemic inflammation, transfusion and mechanical ventilation-related factors. Optimal management requires a multifaceted approach that balances lung-protective ventilation strategies, hemodynamic stability and supportive interventions. Positive end-expiratory pressure (PEEP) and prone positioning improve alveolar recruitment, ventilation homogeneity and oxygenation, moderating ventilator-induced lung injury (VILI). Extracorporeal membrane oxygenation (ECMO), particularly veno-venous ECMO, provides a rescue strategy in refractory hypoxemia but carries significant bleeding risks in multi-trauma patients due to necessary anticoagulation. Fluid management remains critical: both overload and excessive restriction can exacerbate pulmonary compromise or hemodynamic instability. Transfusion practices, including the timing and volume of blood products, significantly influence ARDS development, with blunt thoracic trauma, emergent surgery and high BMI identified as independent risk factors. Despite the progress that has been made, the heterogeneity of ARDS pathophysiology and patient's specific variables necessitate individualized, multidisciplinary management to optimize outcomes in critically ill, trauma patients.

miRNA-149-5p protects endothelial function and attenuates sepsis-induced acute lung injury by targeting ABCA1.

Polysaccharide from Tetrastigma hemsleyanum Diels et Gilg attenuates Poly(I:C)-induced acute lung injury by preserving epithelial barrier integrity and modulating STING/TBK1-NF-κB and IRF1-STAT1 signaling.

Mulberroside A inhibits NLRP6 to prevent alveolar macrophage efferocytosis and lung-derived SAA3-platelet transport in high fructose-induced hippocampal inflammation.

Platycodin D alleviates idiopathic pulmonary fibrosis by targeting PPP2R1A and regulating the PP2A-mediated PI3K/Akt pathway to inhibit fibroblast transdifferentiation.

To investigate the therapeutic mechanisms of Sanhuang Xiexin Decoction (SHXXD) in treating severe acute pancreatitis-associated lung injury (PALI) by modulating the NF-κB signaling pathway. Active components and potential targets of SHXXD were identified through the TCMSP database. A protein-protein interaction (PPI) network was constructed, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis. In vivo and in vitro experiments were performed to evaluate the anti-inflammatory effects of SHXXD in CAE-induced and LPS-induced mouse models and cellular experiments. NF-κB pathway activation and inflammatory cytokine expression were analyzed by Western blot and Quantitative Real-Time PCR (qPCR). Fifty-two active components of SHXXD were identified, including quercetin, baicalin, emodin, and berberine. On the basis of molecular docking results, these components were found to bind strongly with key inflammatory proteins, such as TNF, IL6, IL1B, and MMP9. In vivo experiments showed significant reductions in serum amylase and lipase levels and inhibited NF-κB pathway activation and inflammatory cytokine expression. SHXXD exerts therapeutic effects in treating severe acute pancreatitis-associated lung injury by modulating the NF-κB signaling pathway, making it a potential alternative treatment for PALI. Its active components, including quercetin and baicalin, reduce inflammation.

Ginkgetin alleviates sepsis-induced acute lung injury by promoting autophagy via inhibiting ubiquitination of Laptm5 in macrophages.

Withanolides from Physalis minima as potential anti-inflammatory agents: From isolation to in vitro and in vivo validation.