<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Liao S</submitter><funding>NHLBI NIH HHS</funding><pagination>106-20</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC1852491</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>42(1)</volume><pubmed_abstract>&lt;h4>Unlabelled&lt;/h4>Our laboratory showed that overexpression of fibroblast growth factor-2 (FGF2) protected the heart against ischemia-reperfusion injury. FGF2 has different protein isoforms (low [LMW] and high [HMW] molecular weight isoforms) produced from alternative translation start sites. However, which FGF2 isoform(s) mediates this cardioprotection, and which signaling pathway (i.e., mitogen-activated protein kinase (MAPK)) elicits FGF2 isoform-induced cardioprotection remains to be elucidated.&lt;h4>Methods and results&lt;/h4>Wildtype, Fgf2 KO (absence of all FGF2 isoforms) and FGF2 LMWKO (absence of LMW isoform) hearts were subjected to an ex vivo work-performing heart ischemic model of 60 min ischemia and 120 min reperfusion. There was a significant decrease in the recovery of post-isch</pubmed_abstract><journal>Journal of molecular and cellular cardiology</journal><pubmed_title>The cardioprotective effect of the low molecular weight isoform of fibroblast growth factor-2: the role of JNK signaling.</pubmed_title><pmcid>PMC1852491</pmcid><funding_grant_id>R01 HL075633</funding_grant_id><funding_grant_id>R56 HL075633</funding_grant_id><funding_grant_id>R01 HL070174</funding_grant_id><pubmed_authors>Schultz Jel J</pubmed_authors><pubmed_authors>Scott A</pubmed_authors><pubmed_authors>Liao S</pubmed_authors><pubmed_authors>Doetschman T</pubmed_authors><pubmed_authors>Porter D</pubmed_authors><pubmed_authors>Newman G</pubmed_authors></additional><is_claimable>false</is_claimable><name>The cardioprotective effect of the low molecular weight isoform of fibroblast growth factor-2: the role of JNK signaling.</name><description>&lt;h4>Unlabelled&lt;/h4>Our laboratory showed that overexpression of fibroblast growth factor-2 (FGF2) protected the heart against ischemia-reperfusion injury. FGF2 has different protein isoforms (low [LMW] and high [HMW] molecular weight isoforms) produced from alternative translation start sites. However, which FGF2 isoform(s) mediates this cardioprotection, and which signaling pathway (i.e., mitogen-activated protein kinase (MAPK)) elicits FGF2 isoform-induced cardioprotection remains to be elucidated.&lt;h4>Methods and results&lt;/h4>Wildtype, Fgf2 KO (absence of all FGF2 isoforms) and FGF2 LMWKO (absence of LMW isoform) hearts were subjected to an ex vivo work-performing heart ischemic model of 60 min ischemia and 120 min reperfusion. There was a significant decrease in the recovery of post-isch</description><dates><release>2007-01-01T00:00:00Z</release><publication>2007 Jan</publication><modification>2025-04-04T07:10:29.767Z</modification><creation>2019-06-06T14:03:40Z</creation></dates><accession>S-EPMC1852491</accession><cross_references><pubmed>17150229</pubmed><doi>10.1016/j.yjmcc.2006.10.005</doi></cross_references></HashMap>