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PLA2G7 has been identified as a pathogenic gene in COPD, yet the molecular mechanisms by which PLA2G7 contributes to disease development remain to be elucidated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>To investigate the role of PLA2G7 in obesity-related chronic obstructive pulmonary disease (COPD), we employed clinical specimens as well as in vivo and in vitro models, integrating multi-omics approaches with genetic and pharmacological interventions. Key methodologies included protein and gene expression analyses (Western blotting,, immunohistochemistry, ELISA assay, qRT-PCR), assessment of oxidative stress and lipid peroxidation (ROS and BODIPY staining), histological evaluation (H&amp;E Staining, Oil Red O Staining, AB-PAS staining), transmission electron microscopy, micro-computed tomography (micro-CT), and pulmonary function tests in mice. Furthermore, molecular docking and molecular dynamics simulations were performed to explore potential molecular interactions of PLA2G7.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Using a diet-induced obesity model, this study revealed that obesity alone elicits COPD-like pulmonary changes, defined by weight-dependent alveolar injury, elevated airway mucus secretion, and reduced lung function. Transcriptomic analysis of lung tissues from obesity-associated COPD patients and obese mice identified macrophage-derived phospholipase A2 group VII (\n                      <jats:italic>PLA2G7<\/jats:italic>\n                      ) as a key regulator of disease pathogenesis. Genetic deletion or pharmacological suppression of\n                      <jats:italic>PLA2G7<\/jats:italic>\n                      was found to reduce obesity-associated COPD-like pathology. Mechanistically, high-fat stimulation induced upregulation of\n                      <jats:italic>PLA2G7<\/jats:italic>\n                      in macrophages, leading to increased release of arachidonic acid (AA). The higher AA levels promoted the accumulation of lipid-derived reactive oxygen species (ROS) and stabilized\n                      <jats:italic>NLRP3<\/jats:italic>\n                      mRNA by reducing its degradation. This process activated the inflammasome and triggered pyroptosis, thus driving pulmonary inflammation and contributing to COPD development.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      <jats:italic>PLA2G7<\/jats:italic>\n                      acts as a key mediator of obesity-associated COPD and represents a promising therapeutic target for preventing obesity-related lung injury.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1186\/s12931-026-03540-6","type":"journal-article","created":{"date-parts":[[2026,2,6]],"date-time":"2026-02-06T10:26:44Z","timestamp":1770373604000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Targeting PLA2G7 ameliorates high-fat diet\u2013induced pulmonary injury in obese mice, uncovering a key mechanistic link to obesity-associated COPD"],"prefix":"10.1186","volume":"27","author":[{"given":"Zhi-Heng","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mei-Yu","family":"Lv","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin","family":"Zhang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bao-cai","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yao","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li-Xia","family":"Qiang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiangshun","family":"Li","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenchao","family":"Shi","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xin-yu","family":"Guo","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xi-Qiao","family":"Sang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,2,6]]},"reference":[{"issue":"1","key":"3540_CR1","doi-asserted-by":"publisher","first-page":"93","DOI":"10.1186\/s12931-025-03166-0","volume":"26","author":"LM Paulin","year":"2025","unstructured":"Paulin LM, Halenar MJ, Edwards KC, Lauten K, Stanton CA, Taylor K, et al. 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