{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,17]],"date-time":"2026-08-17T14:45:17Z","timestamp":1786977917836,"version":"build-2736575974"},"reference-count":50,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2019,4,5]],"date-time":"2019-04-05T00:00:00Z","timestamp":1554422400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2019,4,5]],"date-time":"2019-04-05T00:00:00Z","timestamp":1554422400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"name":"Hubei Province Technology Innovation Special","award":["No. 2016ACA153"],"award-info":[{"award-number":["No. 2016ACA153"]}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>The timely regulation of inflammatory M1 macrophage polarization toward regenerative M2 macrophages suggests the possibility of immunotherapy after myocardial infarction (MI). C1q\/TNF\u2010related protein\u20109 (CTRP9) has anti\u2010inflammatory effects and can ameliorate heart function in mice after long\u2010term myocardial infarction. The role of CTRP9 in macrophage polarization remains completely unclear. This study determined whether CTRP9 can preserve post\u2010MI early cardiac function through the regulation of macrophage polarization. In the present study, an adenovirus\u2010delivered CTRP9 supplement promoted macrophage polarization at Day 3 post MI and improved cardiac function at Day 7 post MI. Pretreatment with gCTRP9 promoted the M1 to M2 polarization transition and attenuated inflammation after lipopolysaccharide\u2009+\u2009interferon\u2010\u03b3 stimulation; the effects were partly abrogated by the adenosine monophosphate kinase (AMPK) inhibitor compound C and were obviously reinforced by pyrrolidine dithiocarbamate, a nuclear factor\u2010\u03baB (NF\u2010\u03baB) inhibitor. Meanwhile, CTPR9 markedly reduced the expression of toll\u2010like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and NF\u2010\u03baB p65 phosphorylation by promoting AMPK phosphorylation in vivo and in vitro. Moreover, the competitive binding of gCTRP9 and LPS to the myeloid differentiation protein 2 (MD2)\/TLR4 complex was associated with direct binding to MD2, thereby inhibiting the downstream signaling molecule MyD88. Taken together, we demonstrated that CTRP9 improved post\u2010MI early cardiac function, at least in part, by modulating M1\/M2 macrophage polarization, largely via the TLR4\/MD2\/MyD88 and AMPK\u2010NF\u2010\u03baB pathways.<\/jats:p>","DOI":"10.1002\/jcp.28513","type":"journal-article","created":{"date-parts":[[2019,4,6]],"date-time":"2019-04-06T07:12:30Z","timestamp":1554534750000},"page":"18731-18747","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":51,"title":["C1q\/TNF\u2010related protein\u20109 promotes macrophage polarization and improves cardiac dysfunction after myocardial infarction"],"prefix":"10.1002","volume":"234","author":[{"given":"Mingxin","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Cardiology Renmin Hospital of Wuhan University Wuhan Hubei China"},{"name":"Cardiovascular Research Institute of Wuhan University Wuhan Hubei China"},{"name":"Hubei Key Laboratory of Cardiology Wuhan 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