<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Tan Y</submitter><funding>Key Technologies Research and Development Program</funding><funding>Key Research and Development Projects of Shaanxi Province</funding><funding>National Natural Science Foundation of China</funding><pagination>300</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11892279</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>23(1)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>In developed nations, myocardial infarction (MI) is one of the main causes of morbidity and mortality, resulting in a significant economic burden and becoming a global public health problem. C1q/tumor necrosis factor-related protein 9 (CTRP9) is a secreted protein comprising a variable domain, a collagenous region, and a C-terminal trimerizing globular C1q (gC1q) domain. In vivo, the full-length CTRP9 (fCTRP9) can be cleaved into the globular domain of CTRP9 (gCTRP9). Here, we tested the cardio-protective impacts of fCTRP9, gCTRP9, and N-terminal domain, including the variable and collagenous domain, of CTRP9 (nCTRP9) in the context of MI.&lt;h4>Methods&lt;/h4>Studies comparing the protective properties of fCTRP9 and gCTRP9 against MI in mice hearts were performed both in vitr</pubmed_abstract><journal>Journal of translational medicine</journal><pubmed_title>N-terminal domain of CTRP9 promotes cardiac fibroblast activation in myocardial infarction via Rap1/Mek/Erk pathway.</pubmed_title><pmcid>PMC11892279</pmcid><funding_grant_id>2023-ZDLSF-39</funding_grant_id><funding_grant_id>82170336</funding_grant_id><funding_grant_id>82270286</funding_grant_id><funding_grant_id>81870266</funding_grant_id><funding_grant_id>2022YFC2402804</funding_grant_id><funding_grant_id>82000227</funding_grant_id><pubmed_authors>Li H</pubmed_authors><pubmed_authors>Liu Y</pubmed_authors><pubmed_authors>Shi L</pubmed_authors><pubmed_authors>Cao G</pubmed_authors><pubmed_authors>Zhang Y</pubmed_authors><pubmed_authors>Tan Y</pubmed_authors><pubmed_authors>Yan D</pubmed_authors><pubmed_authors>Li P</pubmed_authors><pubmed_authors>Zhang B</pubmed_authors><pubmed_authors>Yi W</pubmed_authors><pubmed_authors>Sun Y</pubmed_authors><pubmed_authors>Xin J</pubmed_authors></additional><is_claimable>false</is_claimable><name>N-terminal domain of CTRP9 promotes cardiac fibroblast activation in myocardial infarction via Rap1/Mek/Erk pathway.</name><description>&lt;h4>Background&lt;/h4>In developed nations, myocardial infarction (MI) is one of the main causes of morbidity and mortality, resulting in a significant economic burden and becoming a global public health problem. C1q/tumor necrosis factor-related protein 9 (CTRP9) is a secreted protein comprising a variable domain, a collagenous region, and a C-terminal trimerizing globular C1q (gC1q) domain. In vivo, the full-length CTRP9 (fCTRP9) can be cleaved into the globular domain of CTRP9 (gCTRP9). Here, we tested the cardio-protective impacts of fCTRP9, gCTRP9, and N-terminal domain, including the variable and collagenous domain, of CTRP9 (nCTRP9) in the context of MI.&lt;h4>Methods&lt;/h4>Studies comparing the protective properties of fCTRP9 and gCTRP9 against MI in mice hearts were performed both in vitr</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Mar</publication><modification>2025-04-26T02:52:27.046Z</modification><creation>2025-04-06T10:36:02.343Z</creation></dates><accession>S-EPMC11892279</accession><cross_references><pubmed>40065407</pubmed><doi>10.1186/s12967-025-06274-z</doi></cross_references></HashMap>