{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Qi L"],"funding":["China Scholarship Council","NCCIH NIH HHS","NHLBI NIH HHS","National Institute of Health","American Diabetes Association","NIGMS NIH HHS"],"pagination":["59-73"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC7483359"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["145"],"pubmed_abstract":["Deubiquitinating enzymes (DUBs) appear to be a new class of regulators of cardiac homeostasis and disease. However, DUB-mediated signaling in the heart is not well understood. Herein we report a novel mechanism by which cylindromatosis (CYLD), a DUB mediates cardiac pathological remodeling and dysfunction. Cardiomyocyte-restricted (CR) overexpression of CYLD (CR-CYLD) did not cause gross health issues and hardly affected cardiac function up to age of one year in both female and male mice at physiological conditions. However, CR-CYLD overexpression exacerbated pressure overload (PO)-induced cardiac dysfunction associated with suppressed cardiac hypertrophy and increased myocardial apoptosis in mice independent of the gender. At the molecular level, CR-CYLD overexpression enhanced PO-induced"],"journal":["Journal of molecular and cellular cardiology"],"pubmed_title":["CYLD exaggerates pressure overload-induced cardiomyopathy via suppressing autolysosome efflux in cardiomyocytes."],"pmcid":["PMC7483359"],"funding_grant_id":["201506220204","R01 HL085629","1–16-IBS-059","P20 GM103641","R01 HL072166","P01 AT003961","R01 HL131667"],"pubmed_authors":["Qi L","Zang H","Nagarkatti M","Liu Q","Wang X","Wu W","Nagarkatti P","Robbins J","Cui T"],"additional_accession":[]},"is_claimable":false,"name":"CYLD exaggerates pressure overload-induced cardiomyopathy via suppressing autolysosome efflux in cardiomyocytes.","description":"Deubiquitinating enzymes (DUBs) appear to be a new class of regulators of cardiac homeostasis and disease. However, DUB-mediated signaling in the heart is not well understood. Herein we report a novel mechanism by which cylindromatosis (CYLD), a DUB mediates cardiac pathological remodeling and dysfunction. Cardiomyocyte-restricted (CR) overexpression of CYLD (CR-CYLD) did not cause gross health issues and hardly affected cardiac function up to age of one year in both female and male mice at physiological conditions. However, CR-CYLD overexpression exacerbated pressure overload (PO)-induced cardiac dysfunction associated with suppressed cardiac hypertrophy and increased myocardial apoptosis in mice independent of the gender. At the molecular level, CR-CYLD overexpression enhanced PO-induced","dates":{"release":"2020-01-01T00:00:00Z","publication":"2020 Aug","modification":"2026-05-07T15:15:34.208Z","creation":"2022-02-11T00:44:53.787Z"},"accession":"S-EPMC7483359","cross_references":{"pubmed":["32553594"],"doi":["10.1016/j.yjmcc.2020.06.004"]}}