{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Auguste G"],"funding":["NHLBI NIH HHS","NIH HHS"],"pagination":["678-692"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5834384"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["122(5)"],"pubmed_abstract":["RATIONALE:Mutations in the LMNA gene, encoding nuclear inner membrane protein lamin A/C, cause distinct phenotypes, collectively referred to as laminopathies. Heart failure, conduction defects, and arrhythmias are the common causes of death in laminopathies. OBJECTIVE:The objective of this study was to identify and therapeutically target the responsible mechanism(s) for cardiac phenotype in laminopathies. METHODS AND RESULTS:Whole-heart RNA sequencing was performed before the onset of cardiac dysfunction in the Lmna-/- and matched control mice. Differentially expressed transcripts and their upstream regulators were identified, validated, and targeted by adeno-associated virus serotype 9-short hairpin RNA constructs. A total of 576 transcripts were upregulated and 233 were downregulated in "],"journal":["Circulation research"],"pubmed_title":["Suppression of Activated FOXO Transcription Factors in the Heart Prolongs Survival in a Mouse Model of Laminopathies."],"pmcid":["PMC5834384"],"funding_grant_id":["R01 HL117641","R01 HL132401","R01 HL091947","S10 OD018135","R41 HL129570","R01 HL088498","R01 HL089598"],"pubmed_authors":["Auguste G","Gurha P","Coarfa C","Marian AJ","Willerson JT","Lombardi R"],"additional_accession":[]},"is_claimable":false,"name":"Suppression of Activated FOXO Transcription Factors in the Heart Prolongs Survival in a Mouse Model of Laminopathies.","description":"RATIONALE:Mutations in the LMNA gene, encoding nuclear inner membrane protein lamin A/C, cause distinct phenotypes, collectively referred to as laminopathies. Heart failure, conduction defects, and arrhythmias are the common causes of death in laminopathies. OBJECTIVE:The objective of this study was to identify and therapeutically target the responsible mechanism(s) for cardiac phenotype in laminopathies. METHODS AND RESULTS:Whole-heart RNA sequencing was performed before the onset of cardiac dysfunction in the Lmna-/- and matched control mice. Differentially expressed transcripts and their upstream regulators were identified, validated, and targeted by adeno-associated virus serotype 9-short hairpin RNA constructs. A total of 576 transcripts were upregulated and 233 were downregulated in ","dates":{"release":"2018-01-01T00:00:00Z","publication":"2018 Mar","modification":"2025-04-19T15:19:45.812Z","creation":"2019-08-04T07:29:49Z"},"accession":"S-EPMC5834384","cross_references":{"pubmed":["29317431"],"doi":["10.1161/circresaha.117.312052","10.1161/CIRCRESAHA.117.312052"]}}