{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T04:08:45Z","timestamp":1789013325911,"version":"build-2803163510"},"reference-count":45,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"15","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,8,4]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Both hyperlipidemia and chronic pain were recognized risk factors for cardiac injury, which could lead to cardiovascular diseases.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">Thirty\u2010two male APOE\u2212\/\u2212 (apolipoprotein E\u2010deficient) mice (C57BL\/6 background, 1 month old) were randomly allocated to 4 groups (n=8\/group): Sham group: high\u2010fat diet+sham surgery for 3 months; P1 to P3 groups: high\u2010fat diet +spared nerve injury\u2010induced chronic pain initiated at 1, 2, or 3 months post high\u2010fat diet commencement, respectively. Mechanical allodynia was induced via the spared nerve injury model. Pain thresholds were quantified using von Frey filaments. Anxiety\u2010like behaviors were assessed via the Open Field Test. Transthoracic echocardiography was performed to measure left ventricular ejection fraction and fractional shortening. Serum biomarkers of myocardial injury, inflammatory cytokines and lipid profiles were analyzed by ELISA. Myocardial tissue sections were subjected to histopathological staining, immunohistochemistry, immunofluorescence, and Western blotting.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Chronic pain exerted negligible effects on high\u2010fat diet\u2010induced metabolic dysregulation, as evidenced by comparable levels of total cholesterol, low\u2010density lipoprotein cholesterol, and triglycerides across all groups (\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      &gt;0.05). In contrast, mice subjected to chronic pain (P1\u2013P3 groups) exhibited significant deterioration in myocardial contractility, exacerbated fibrosis and collagen deposition, elevated cardiac injury biomarkers, and pronounced inflammatory cell infiltration compared with Sham group. These alterations correlated with dysregulated JNK1 (c\u2010Jun N\u2010terminal kinase 1) activation and suppressed Sirt1 (silent information regulator 1) expression in myocardial tissues.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">These findings demonstrated that chronic pain synergistically exacerbated hyperlipidemia\u2010induced cardiac injury, primarily mediated through inflammatory mechanisms and JNK1\/Sirt1 signaling dysregulation.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.125.045604","type":"journal-article","created":{"date-parts":[[2026,7,31]],"date-time":"2026-07-31T11:13:50Z","timestamp":1785496430000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":0,"title":["Chronic Pain Synergizes With High\u2010Fat Diet to Promote Cardiac Injury via c\u2010Jun N\u2010Terminal Kinase 1\/Silent Information Regulator 1 Signaling Axis in Apolipoprotein E\u2010Deficient Mice"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9514-6138","authenticated-orcid":false,"given":"Lan","family":"Wei","sequence":"first","affiliation":[{"name":"Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University","place":["Shanghai, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiang","family":"Tao","sequence":"additional","affiliation":[{"name":"The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai Jiao Tong University","place":["Shanghai, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shan","family":"You","sequence":"additional","affiliation":[{"name":"Shanghai General Hospital, School of Medicine, Shanghai Jiao Tong University","place":["Shanghai, 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