<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Bhandari P</submitter><funding>NHLBI NIH HHS</funding><pagination>257-65</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4392818</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>114(2)</volume><pubmed_abstract>&lt;h4>Rationale&lt;/h4>Dysfunctional Parkin-mediated mitophagic culling of senescent or damaged mitochondria is a major pathological process underlying Parkinson disease and a potential genetic mechanism of cardiomyopathy. Despite epidemiological associations between Parkinson disease and heart failure, the role of Parkin and mitophagic quality control in maintaining normal cardiac homeostasis is poorly understood.&lt;h4>Objective&lt;/h4>We used germline mutants and cardiac-specific RNA interference to interrogate Parkin regulation of cardiomyocyte mitochondria and examine functional crosstalk between mitophagy and mitochondrial dynamics in Drosophila heart tubes.&lt;h4>Methods and results&lt;/h4>Transcriptional profiling of Parkin knockout mouse hearts revealed compensatory upregulation of multiple relate</pubmed_abstract><journal>Circulation research</journal><pubmed_title>Mitochondrial contagion induced by Parkin deficiency in Drosophila hearts and its containment by suppressing mitofusin.</pubmed_title><pmcid>PMC4392818</pmcid><funding_grant_id>R01 HL059888</funding_grant_id><funding_grant_id>R21 HL107276</funding_grant_id><funding_grant_id>HL107276</funding_grant_id><funding_grant_id>HL59888</funding_grant_id><pubmed_authors>Song M</pubmed_authors><pubmed_authors>Dorn GW</pubmed_authors><pubmed_authors>Chen Y</pubmed_authors><pubmed_authors>Burelle Y</pubmed_authors><pubmed_authors>Bhandari P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Mitochondrial contagion induced by Parkin deficiency in Drosophila hearts and its containment by suppressing mitofusin.</name><description>&lt;h4>Rationale&lt;/h4>Dysfunctional Parkin-mediated mitophagic culling of senescent or damaged mitochondria is a major pathological process underlying Parkinson disease and a potential genetic mechanism of cardiomyopathy. Despite epidemiological associations between Parkinson disease and heart failure, the role of Parkin and mitophagic quality control in maintaining normal cardiac homeostasis is poorly understood.&lt;h4>Objective&lt;/h4>We used germline mutants and cardiac-specific RNA interference to interrogate Parkin regulation of cardiomyocyte mitochondria and examine functional crosstalk between mitophagy and mitochondrial dynamics in Drosophila heart tubes.&lt;h4>Methods and results&lt;/h4>Transcriptional profiling of Parkin knockout mouse hearts revealed compensatory upregulation of multiple relate</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Jan</publication><modification>2025-04-18T19:17:43.268Z</modification><creation>2019-03-26T23:49:36Z</creation></dates><accession>S-EPMC4392818</accession><cross_references><pubmed>24192653</pubmed><doi>10.1161/CIRCRESAHA.114.302734</doi><doi>10.1161/circresaha.114.302734</doi></cross_references></HashMap>