{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhou C"],"funding":["Ningbo Top Medical and Health Research Program","Natural Science Foundation of Shanghai Municipality","National Natural Science Foundation of China","Medical and Health Technology Plan Projects of Zhejiang"],"pagination":["1075"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11604012"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["22(1)"],"pubmed_abstract":["Background
Right ventricular volume overload (RVVO) is one of the most important hemodynamic characteristics in children with congenital heart disease (CHD) and heart failure, and cardiomyocyte (CM) proliferation is one of the most vital factors for improving cardiac performance. However, whether and how RVVO reboots CM proliferation remains elusive.Methods and results
We first created a neonatal RVVO mouse model via abdominal aorta and inferior vena cava-fistula microsurgery at postnatal day 7 (P7), the edge of CM proliferation window. We subsequently performed bulk RNA-seq, single cell RNA-seq/flow cytometry, and immunofluorescence staining on the right ventricles (RV) of RVVO mice at P14/P21, defined as prepubertal stage, revealing that RVVO temporarily reboots prepubert"],"journal":["Journal of translational medicine"],"pubmed_title":["Right ventricular volume overload reboots cardiomyocyte proliferation via immune responses."],"pmcid":["PMC11604012"],"funding_grant_id":["No. 2022020405","No.82200309","2024YK1568","No. 82270314","No. 22ZR1479900 and No. 23ZR1441100"],"pubmed_authors":["Ye L","Hu Y","Li D","Zhou C","Dong Z","Xiao Y","Sun S","Zhang H","Zheng S","Chen H","Wang Z","Chen D"],"additional_accession":[]},"is_claimable":false,"name":"Right ventricular volume overload reboots cardiomyocyte proliferation via immune responses.","description":"Background
Right ventricular volume overload (RVVO) is one of the most important hemodynamic characteristics in children with congenital heart disease (CHD) and heart failure, and cardiomyocyte (CM) proliferation is one of the most vital factors for improving cardiac performance. However, whether and how RVVO reboots CM proliferation remains elusive.Methods and results
We first created a neonatal RVVO mouse model via abdominal aorta and inferior vena cava-fistula microsurgery at postnatal day 7 (P7), the edge of CM proliferation window. We subsequently performed bulk RNA-seq, single cell RNA-seq/flow cytometry, and immunofluorescence staining on the right ventricles (RV) of RVVO mice at P14/P21, defined as prepubertal stage, revealing that RVVO temporarily reboots prepubert","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Nov","modification":"2026-07-15T09:34:32.582Z","creation":"2025-04-04T02:33:07.823Z"},"accession":"S-EPMC11604012","cross_references":{"pubmed":["39609689"],"doi":["10.1186/s12967-024-05839-8"]}}