{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T01:01:14Z","timestamp":1792112474783,"version":"4.4.0"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T00:00:00Z","timestamp":1771977600000},"content-version":"vor","delay-in-days":24,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"},{"start":{"date-parts":[[2026,2,1]],"date-time":"2026-02-01T00:00:00Z","timestamp":1769904000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2026,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Coronary heart disease (CHD) may worsen anaphylactic shock, but the exact mechanism is unknown. This study aimed to investigate the mechanisms by which coronary heart disease exacerbates anaphylaxis.C57BL\/6 (WT) mice and LDLR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were fed a high\u2010fat diet for 20 weeks to develop atherosclerosis. Anaphylaxis was then induced using ovalbumin (OVA). Compared to WT mice, LDLR\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice showed lower body temperature, worse pulmonary edema and higher mortality. Pulmonary endothelial cell CD31 (PECAM\u20101) expression decreased, but serum HMGB\u20101 levels increased. In vitro experiments found that ox\u2010LDL exposure led to more HMGB\u20101 release from HUVECs. Moreover, ox\u2010LDL induced mast cells release of histamine, upregulating the expression of more H1 receptors (H1R) in HUVECs, thereby further promoting HMGB\u20101 release. Pretreatment with an H1R inhibitor (chlorpheniramine) or an HMGB\u20101 neutralizing antibody improved survival and attenuated hypothermia in mice. In summary, ox\u2010LDL exacerbates endothelial cell damage, resulting in increased HMGB\u20101 release and vascular permeability, which may worsen anaphylaxis to anaphylactic shock. The mechanisms are not fully understood, but HMGB\u20101 could be a potential target for future alleviation of anaphylactic shock.\n                  <\/jats:p>","DOI":"10.1002\/jcp.70154","type":"journal-article","created":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T11:03:17Z","timestamp":1772967797000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["HMGB\u20101 Mediates The Exacerbation of Anaphylactic Shock Under Hyperlipidemic Conditions"],"prefix":"10.1002","volume":"241","author":[{"given":"Zikang","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Forensic Medicine, School of Basic Medical Sciences Harbin Medical University Harbin Heilongjiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tingting","family":"Ding","sequence":"additional","affiliation":[{"name":"Department of Forensic Medicine, School of Basic Medical Sciences Harbin Medical University 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