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Hypothalamic pro\u2010opiomelanocortin\u2010expressing (POMC+) neurons regulate systemic metabolic homeostasis, and tripartite motif\u2010containing protein 31 (TRIM31) modulates inflammation and metabolism. Here, we investigated whether TRIM31 in POMC+ neurons mediates PM\n                    <jats:sub>2.5<\/jats:sub>\n                    \u2010induced hypothalamic injury and peripheral metabolic disorders in mice subjected to 24\u2010week PM\n                    <jats:sub>2.5<\/jats:sub>\n                    exposure. TRIM31 knockout in POMC\n                    <jats:sup>+<\/jats:sup>\n                    neurons (\n                    <jats:italic>\n                      POMC\n                      <jats:sup>Cre\/+;<\/jats:sup>\n                      TRIM31\n                      <jats:sup>flox\/flox<\/jats:sup>\n                    <\/jats:italic>\n                    ) exacerbated PM\n                    <jats:sub>2.5<\/jats:sub>\n                    \u2010;induced increases in mean blood pressure and fat weight, liver weight reduction, adipocyte hypertrophy, hepatic lipid deposition, energy expenditure abnormalities and insulin resistance. It also aggravated hypothalamic damage (downregulated NeuN, POMC and MC4R) and amplified neuroinflammation and oxidative stress. Conversely, AAV\u2010mediated TRIM31 overexpression in POMC\n                    <jats:sup>+<\/jats:sup>\n                    neurons alleviated these pathological phenotypes. In vitro, TRIM31 deletion promoted reactive oxygen species (ROS) and inflammation in PM\n                    <jats:sub>2.5<\/jats:sub>\n                    \u2010challenged hypothalamic neurons and microglia, while TRIM31 overexpression exerted opposite effects; microglial TRIM31 depletion exacerbated neuronal death via conditioned medium. Mechanistically, TRIM31 directly interacted with Nrf2, enhancing its K63\u2010linked polyubiquitination and reducing K48\u2010linked polyubiquitination to activate Nrf2 signaling, which was required for TRIM31\u2010mediated attenuation of neuronal death and inflammation under PM2.5 stress. Collectively, our findings identify the TRIM31\/Nrf2 axis as a key molecular switch governing POMC\n                    <jats:sup>+<\/jats:sup>\n                    neuronal loss, hypothalamic injury and consequent peripheral metabolic disorders triggered by long\u2010term PM\n                    <jats:sub>2.5<\/jats:sub>\n                    exposure.\n                  <\/jats:p>","DOI":"10.1002\/advs.202508458","type":"journal-article","created":{"date-parts":[[2026,1,10]],"date-time":"2026-01-10T04:06:01Z","timestamp":1768017961000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Dysfunctional TRIM31 of POMC Neurons Provokes Hypothalamic Injury and Peripheral Metabolic Disorder under Long\u2010Term Fine Particulate Matter Exposure"],"prefix":"10.1002","volume":"13","author":[{"given":"Chenxu","family":"Ge","sequence":"first","affiliation":[{"name":"Key Laboratory of Biorheological Science and Technology (Chongqing University) Ministry of Education Chongqing University  Chongqing P. 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