{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,1]],"date-time":"2026-09-01T15:27:46Z","timestamp":1788276466166,"version":"build-2803163510"},"reference-count":30,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2026,3,23]],"date-time":"2026-03-23T00:00:00Z","timestamp":1774224000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,3,23]],"date-time":"2026-03-23T00:00:00Z","timestamp":1774224000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100007129","name":"Natural Science Foundation of Shandong Province","doi-asserted-by":"publisher","award":["ZR2021MH091"],"award-info":[{"award-number":["ZR2021MH091"]}],"id":[{"id":"10.13039\/501100007129","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100018546","name":"Postdoctoral Innovation Project of Shandong Province","doi-asserted-by":"publisher","award":["SDCX\u2010ZG\u2010202303095"],"award-info":[{"award-number":["SDCX\u2010ZG\u2010202303095"]}],"id":[{"id":"10.13039\/501100018546","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["analyticalsciencejournals.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Applied Toxicology"],"published-print":{"date-parts":[[2026,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>Epidemiological studies link fine particulate matter (PM2.5) exposure to aggravated viral myocarditis (VMC), though the mechanisms remain unclear. This study aimed to investigate whether PM2.5 exacerbates the inflammatory response by disrupting lysophosphatidylcholine (LPC) metabolism and its downstream signaling pathways. We established the mouse model combining PM2.5 exposure and CVB3 infection. Cardiac function, inflammation, and signaling molecule alterations were assessed using echocardiography, histological analysis, and molecular techniques. In H9c2 cardiomyocytes, we applied PM2.5, LPC, GPR4 siRNA, and pathway inhibitors (U0126 and GW9662). PM2.5 reduced LPC levels in\u00a0vivo and in\u00a0vitro and downregulated its receptor GPR4. It also suppressed the ERK\/PPAR\u03b3 pathway, thereby lifting transcriptional inhibition of Toll\u2010like receptor 4 (TLR4). GPR4 knockdown abolished the activating effects of LPC on ERK\/PPAR\u03b3 and its inhibitory effect on TLR4. Our study also confirmed that ERK and PPAR\u03b3 function sequentially downstream of GPR4 and upstream of TLR4 within this pathway. The study suggests a novel mechanism by which PM2.5 exacerbates VMC. PM2.5 disrupts LPC metabolism, inhibits the GPR4\/ERK\/PPAR\u03b3 pathway, and consequently releases the inhibition on TLR4, thereby increasing cardiac susceptibility to CVB3 and inflammatory injury. This pathway represents a potential therapeutic target for preventing PM2.5\u2010associated myocardial damage.<\/jats:p>","DOI":"10.1002\/jat.70180","type":"journal-article","created":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T06:41:05Z","timestamp":1774334465000},"page":"3455-3464","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["PM2.5 Exacerbates Viral Myocarditis by Disrupting Lysophosphatidylcholine Metabolism and Inhibiting the GPR4\/ERK\/PPAR\u03b3 Pathway"],"prefix":"10.1002","volume":"46","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-6719-5315","authenticated-orcid":false,"given":"Diandian","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Ultrasound Shandong Provincial Hospital Affiliated to Shandong First Medical University  Jinan 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