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CQMU-5 is a novel, specific small molecule agonist of the zinc transporter ZIP1 (SLC39A1), currently under investigation for the treatment of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Developed by researchers at Chongqing Medical University, CQMU-5 works by facilitating zinc influx into alveolar type 2 (AT2) cells. This influx activates a signaling pathway involving transcription factors TFEB, TFE3, and MITF, which triggers a protective autophagic response. This mechanism promotes the clearance of damaged mitochondria and inhibits apoptotic and pyroptotic cell death, thereby maintaining lung epithelial integrity. Preclinical studies have demonstrated that CQMU-5 significantly reduces the severity of lung injury in murine models induced by Streptococcus pneumoniae, sepsis, and endotoxins.
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