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Macrophage autophagic homeostasis is essential to constrain septic ALI inflammation, though its upstream regulation remains elusive. Here, we report that lysosomal\u2010associated protein transmembrane 5 (LAPTM5) is markedly downregulated in peripheral blood mononuclear cells (PBMCs) from septic ALI patients and alveolar macrophages (AMs) of septic mice, with its expression correlating inversely with the SOFA score. Macrophage\u2010specific depletion of\n                    <jats:italic>Laptm5<\/jats:italic>\n                    exacerbated mouse ALI symptoms, whereas AAV\u2010mediated\n                    <jats:italic>Laptm5<\/jats:italic>\n                    overexpression yielded diametrically opposite effects. Mechanistically, LPS stimulation promotes FOXB1 nuclear accumulation, which in turn represses the transcription and protein expression of LAPTM5. Furthermore, LAPTM5 acts as a molecular scaffold bridging PGAM5 and VAMP8, mediating PGAM5\u2010dependent VAMP8 dephosphorylation to promote autophagosome\u2010lysosome fusion and autophagic flux. This cascade clears damaged mitochondria, thereby mitigating intracellular oxidative stress and inflammation. This study defines macrophage LAPTM5 as a critical autophagy regulator that mitigates septic ALI, providing a potential avenue for future therapeutic exploration.\n                  <\/jats:p>","DOI":"10.1002\/advs.78024","type":"journal-article","created":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T18:00:31Z","timestamp":1790532031000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["<i>LAPTM5<\/i>\n                    Downregulation\u2010Driven VAMP8 Phosphorylation Impairs Autophagosome\u2010Lysosome Fusion and Aggravates Septic Acute Lung Injury"],"prefix":"10.1002","author":[{"given":"Lang","family":"Jiang","sequence":"first","affiliation":[{"name":"Department of Critical Care Medicine Union Hospital Tongji Medical College Huazhong University of Science and Technology  Wuhan 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