{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,16]],"date-time":"2026-05-16T15:50:46Z","timestamp":1778946646738,"version":"3.51.4"},"reference-count":31,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2020,1,14]],"date-time":"2020-01-14T00:00:00Z","timestamp":1578960000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100011002","name":"National Natural Science Foundation of China-Yunnan Joint Fund","doi-asserted-by":"publisher","award":["#81400352"],"award-info":[{"award-number":["#81400352"]}],"id":[{"id":"10.13039\/501100011002","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clin Exp Pharma Physio"],"published-print":{"date-parts":[[2020,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The therapeutic potential of the antimicrobial peptide cathelicidin (\n                    <jats:italic>Camp<\/jats:italic>\n                    ) administration in sepsis has been widely investigated. However, little is known about the pathophysiological roles of cathelicidin in septic cardiomyopathy. In a lipopolysaccharide (LPS)\u2010induced endotoxaemic model, we found that the mRNA and protein expression of cardiac cathelicidin were induced in C57BL\/6J wild\u2010type (WT) mice upon LPS challenge, accompanied by increased circulating cathelicidin levels. We showed that this peptide was mainly derived from neutrophils and monocytes\/macrophages.\n                    <jats:italic>Camp<\/jats:italic>\n                    deficiency exacerbated LPS\u2010induced myocardial depression, while the administration of CRAMP (the mature form of mouse cathelicidin) decreased the LPS\u2010induced mortality in a D\u2010galactosamine hydrochloride (D\u2010GalN)\u2010sensitized endotoxin shock model. In vivo, LPS\u2010treated\n                    <jats:italic>Camp<\/jats:italic>\n                    knockout mice had a significant higher protein level of myocardial and circulating tumour necrosis factor\u2010alpha (TNF\u2010\u03b1), a major contributing factor to septic cardiomyopathy, compared to LPS\u2010treated WT mice, while CRAMP administration inhibited LPS\u2010induced TNF\u2010\u03b1 production in the heart and plasma in D\u2010GalN\u2010sensitized endotoxaemic mice. In vitro, CRAMP treatment suppressed LPS\u2010induced\n                    <jats:italic>Tnf\u2010\u03b1<\/jats:italic>\n                    mRNA expression in cultured neonatal mouse cardiomyocytes and reduced TNF\u2010\u03b1 secretion in the culture supernatant. The inhibitory effects of CRAMP on TNF\u2010\u03b1 production may be related to its neutralizing ability of LPS, since CRAMP application had no effects on another toll\u2010like receptor 4 ligand paclitaxel\u2010induced\n                    <jats:italic>Tnf\u2010\u03b1<\/jats:italic>\n                    mRNA expression in cardiomyocytes. These findings suggest that LPS\u2010induced cathelicidin protects the heart against myocardial depression partly through the inhibition of TNF\u2010\u03b1 production via neutralizing LPS.\n                  <\/jats:p>","DOI":"10.1111\/1440-1681.13234","type":"journal-article","created":{"date-parts":[[2019,12,23]],"date-time":"2019-12-23T11:18:00Z","timestamp":1577099880000},"page":"677-686","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Cathelicidin deficiency exacerbates cardiac dysfunction in lipopolysaccharide\u2010induced endotoxaemic mice"],"prefix":"10.1111","volume":"47","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0891-4777","authenticated-orcid":false,"given":"Tingting","family":"Zhai","sequence":"first","affiliation":[{"name":"Department of Metabolism and Endocrinology The Second Xiangya Hospital Central South University Changsha Hunan China"},{"name":"National Clinical Research Center for 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