<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Li G</submitter><funding>National Natural Science Foundation of China</funding><funding>Sichuan Science and Technology Program</funding><pagination>e70735</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12318481</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>29(15)</volume><pubmed_abstract>This study aims to elucidate the role of MARCH5 in cardiac hypertrophy, thereby providing a theoretical foundation for novel therapeutic strategies for cardiac hypertrophy and heart failure. The expression of MARCH5 in cardiac hypertrophy models was assessed using immunohistochemistry, western blot (WB) and RT-qPCR. Gain- and loss-of-function experiments of MARCH5 in cardiac hypertrophy were conducted both in vitro and in vivo. WB, RT-qPCR, co-immunoprecipitation (CoIP), immunohistochemistry and immunofluorescence were performed to investigate the molecular mechanisms of MARCH5. MARCH5 expression was upregulated in hypertrophied myocardium. Ang II stimulation resulted in increased expression of MYH7, BNP and cardiomyocyte area. These effects were aggravated by MARCH5 overexpression but ant</pubmed_abstract><journal>Journal of cellular and molecular medicine</journal><pubmed_title>MARCH5 Promotes Cardiac Hypertrophy by Regulating Akt/mTOR/Gsk-3β/GATA4 Signalling Pathway.</pubmed_title><pmcid>PMC12318481</pmcid><funding_grant_id>2023NSFSC1645</funding_grant_id><funding_grant_id>81900348</funding_grant_id><funding_grant_id>2023NSFSC1650</funding_grant_id><pubmed_authors>Li G</pubmed_authors><pubmed_authors>Liao Y</pubmed_authors><pubmed_authors>Zhang J</pubmed_authors><pubmed_authors>Lei F</pubmed_authors><pubmed_authors>Wu F</pubmed_authors></additional><is_claimable>false</is_claimable><name>MARCH5 Promotes Cardiac Hypertrophy by Regulating Akt/mTOR/Gsk-3β/GATA4 Signalling Pathway.</name><description>This study aims to elucidate the role of MARCH5 in cardiac hypertrophy, thereby providing a theoretical foundation for novel therapeutic strategies for cardiac hypertrophy and heart failure. The expression of MARCH5 in cardiac hypertrophy models was assessed using immunohistochemistry, western blot (WB) and RT-qPCR. Gain- and loss-of-function experiments of MARCH5 in cardiac hypertrophy were conducted both in vitro and in vivo. WB, RT-qPCR, co-immunoprecipitation (CoIP), immunohistochemistry and immunofluorescence were performed to investigate the molecular mechanisms of MARCH5. MARCH5 expression was upregulated in hypertrophied myocardium. Ang II stimulation resulted in increased expression of MYH7, BNP and cardiomyocyte area. These effects were aggravated by MARCH5 overexpression but ant</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Aug</publication><modification>2025-08-14T03:05:58.899Z</modification><creation>2025-08-14T03:05:58.899Z</creation></dates><accession>S-EPMC12318481</accession><cross_references><pubmed>40753540</pubmed><doi>10.1111/jcmm.70735</doi></cross_references></HashMap>