{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T18:32:54Z","timestamp":1791311574630,"version":"4.3.1"},"reference-count":90,"publisher":"Wiley","issue":"14","license":[{"start":{"date-parts":[[2025,2,18]],"date-time":"2025-02-18T00:00:00Z","timestamp":1739836800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82360372"],"award-info":[{"award-number":["82360372"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["advanced.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Advanced Science"],"published-print":{"date-parts":[[2025,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Acute lung injury (ALI) refers to damage to lung related cells, typically caused by an uncontrollable inflammatory response, and over\u2010generated reactive oxygen species (ROS). Increasing evidence suggests that reprogramming lung redox homeostasis holds significant potentials for the clinical treatment of ALI. Herein, the simple synthesis of ultra\u2010small Pd loaded covalent organic framework (COF) (TP@Pd) is reported, which, when combined with near infrared (NIR) irradiation, exhibits nanozyme functionalities, including multiple enzyme mimicking activities and broad spectrum ROS scavenging, thereby promoting tissue repair for ALI immunotherapy. Mechanistically, through the therapeutic strategy of TP@Pd+NIR, the damaged cells and tissues are ameliorated by decreasing intracellular ROS levels (total ROS, \u00b7OH and \u00b7O\n                    <jats:sub>2<\/jats:sub>\n                    <jats:sup>\u2212<\/jats:sup>\n                    ), downregulating inflammatory cytokines levels (IL\u20106, TNF\u2010\u03b1 and IL\u20101\u03b2), upregulating antioxidant factor level (SOD2), inducing macrophage M2 directional polarization (downregulation of iNOS and CD86, and upregulation of IL\u201010 and CD206), activating immunoregulation (CD4\n                    <jats:sup>+<\/jats:sup>\n                    \/CD8\n                    <jats:sup>+<\/jats:sup>\n                    ratio increase), promoting tissue repair factor levels (upregulation of HSP70 and CD31), and suppressing the NF\u2010\u03baB signaling pathway (downregulation of phosphorylated p65 and I\u03baB\u03b1). Furthermore, following intravenous (IV) injection in rats, TP@Pd accumulated in lung tissue for 6 h, indicating the promising therapeutic efficacy via this administration route. Notably, the TP@Pd+NIR strategy demonstrated the excellent synergistic effects in alleviating lung inflammation storms, reducing diffuse alveolar damage, and accelerating lung tissue repair. Summarily, this work has designed a novel TP@Pd+NIR strategy for the synergistic enhancement of ALI amelioration, which may serve as a promising therapeutic approach for other ROS related diseases.\n                  <\/jats:p>","DOI":"10.1002\/advs.202413697","type":"journal-article","created":{"date-parts":[[2025,2,18]],"date-time":"2025-02-18T15:13:46Z","timestamp":1739891626000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":31,"title":["Reprogramming Lung Redox Homeostasis by NIR Driven Ultra\u2010Small Pd Loaded Covalent Organic Framework Inhibits NF\u2010\u03baB Pathway for Acute Lung Injury Immunotherapy"],"prefix":"10.1002","volume":"12","author":[{"given":"Doudou","family":"Lei","sequence":"first","affiliation":[{"name":"Intensive Care Unit The Second Affiliated Hospital of Guangxi Medical University  Nanning Guangxi 530\u00a0007 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