{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee S"],"funding":["European Research Council","NHLBI NIH HHS","NIGMS NIH HHS"],"pagination":["1279-1291"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12533503"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["137(10)"],"pubmed_abstract":["Background
Induction of cardiomyocyte proliferation in situ represents a promising strategy for myocardial regeneration following injury. However, cardiomyocytes possess intrinsic inhibitory mechanisms that attenuate pro-proliferative signaling and constrain their expansion. We hypothesized that cell-cell contact is a key suppressor of cardiomyocyte proliferation. We aimed to delineate the underlying molecular pathways to enable sustained proliferation in 3-dimensional contexts.Methods
Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were cultured at varying plating densities to examine the impact of cell-cell contact on cell cycle activity. Phosphoproteomic profiling was performed in sparse versus dense cultures to identify signaling alterations. Cond"],"journal":["Circulation research"],"pubmed_title":["IGFBP2 Mediates Human iPSC-Cardiomyocyte Proliferation in a Cellular Contact-Dependent Manner."],"pmcid":["PMC12533503"],"funding_grant_id":["RM1 GM131981","R01 HL171574","788381","101141820","F32 HL142205"],"pubmed_authors":["Yun J","Lee S","Heinrich P","Robinson HR","Kim B","Hudson JE","Wu SM","Wu JC","Moretti A","Humphrey SJ","Goodyer WR","Lee J","Min S","Paik DT","Kang Y","Lee D","Buikema JW","Cho SW","Belbachir N","Galdos FX"],"additional_accession":[]},"is_claimable":false,"name":"IGFBP2 Mediates Human iPSC-Cardiomyocyte Proliferation in a Cellular Contact-Dependent Manner.","description":"Background
Induction of cardiomyocyte proliferation in situ represents a promising strategy for myocardial regeneration following injury. However, cardiomyocytes possess intrinsic inhibitory mechanisms that attenuate pro-proliferative signaling and constrain their expansion. We hypothesized that cell-cell contact is a key suppressor of cardiomyocyte proliferation. We aimed to delineate the underlying molecular pathways to enable sustained proliferation in 3-dimensional contexts.Methods
Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) were cultured at varying plating densities to examine the impact of cell-cell contact on cell cycle activity. Phosphoproteomic profiling was performed in sparse versus dense cultures to identify signaling alterations. Cond","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-10T05:17:17.96Z","creation":"2026-06-10T03:07:17.375Z"},"accession":"S-EPMC12533503","cross_references":{"pubmed":["41031396"],"doi":["10.1161/CIRCRESAHA.125.326522","10.1161/circresaha.125.326522"]}}