{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Hu YF"],"funding":["National Health Research Institutes","Taipei Veterans General Hospital","Academia Sinica","NIAAA NIH HHS"],"pagination":["166088"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC8168427"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["1867(5)"],"pubmed_abstract":["Point mutation in alcohol dehydrogenase 2 (ALDH2), ALDH2*2 results in decreased catalytic enzyme activity and has been found to be associated with different human pathologies. Whether ALDH2*2 would induce cardiac remodeling and increase the attack of atrial fibrillation (AF) remains poorly understood. The present study evaluated the effect of ALDH2*2 mutation on AF susceptibility and unravelled the underlying mechanisms using a multi-omics approach including whole-genome gene expression and proteomics analysis. The in-vivo electrophysiological study showed an increase in the incidence and reduction in the threshold of AF for the mutant mice heterozygous for ALDH2*2 as compared to the wild type littermates. The microarray analysis revealed a reduction in the retinoic acid signals which was "],"journal":["Biochimica et biophysica acta. Molecular basis of disease"],"pubmed_title":["ALDH2 deficiency induces atrial fibrillation through dysregulated cardiac sodium channel and mitochondrial bioenergetics: A multi-omics analysis."],"pmcid":["PMC8168427"],"funding_grant_id":["R37 AA011147","R01 AA011147"],"pubmed_authors":["Chang PM","Huang CF","Wu CH","Chang TY","Weng CH","Chen SA","Hu YF","Lai TC","Chen CH","Mochly-Rosen D","Chang YC","Hwang MJ"],"additional_accession":[]},"is_claimable":false,"name":"ALDH2 deficiency induces atrial fibrillation through dysregulated cardiac sodium channel and mitochondrial bioenergetics: A multi-omics analysis.","description":"Point mutation in alcohol dehydrogenase 2 (ALDH2), ALDH2*2 results in decreased catalytic enzyme activity and has been found to be associated with different human pathologies. Whether ALDH2*2 would induce cardiac remodeling and increase the attack of atrial fibrillation (AF) remains poorly understood. The present study evaluated the effect of ALDH2*2 mutation on AF susceptibility and unravelled the underlying mechanisms using a multi-omics approach including whole-genome gene expression and proteomics analysis. The in-vivo electrophysiological study showed an increase in the incidence and reduction in the threshold of AF for the mutant mice heterozygous for ALDH2*2 as compared to the wild type littermates. The microarray analysis revealed a reduction in the retinoic acid signals which was ","dates":{"release":"2021-01-01T00:00:00Z","publication":"2021 May","modification":"2025-04-03T23:16:21.141Z","creation":"2025-02-18T23:32:31.367Z"},"accession":"S-EPMC8168427","cross_references":{"pubmed":["33515676"],"doi":["10.1016/j.bbadis.2021.166088"]}}