{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"volume":["13(1)"],"submitter":["Zhang D"],"pubmed_abstract":["Pyruvate kinase M1 (PKM1) is a critical enzyme in glycolysis, particularly in high-energy-demand tissues like the heart. However, previous knockout strategies for PKM1 were confounded by compensatory upregulation of its low-activity splice variant, PKM2. Here, we generated a <i>Pkm1</i> mutant mouse model using a point mutation that eliminates PKM1 without compensatory PKM2 upregulation. Homozygous <i>Pkm1</i> mutants exhibited perinatal lethality associated with cardiac dysfunction, characterized by thin myocardium and reduced cardiomyocyte proliferation during mid-to-late gestation. We found that PKM1 sustains ATP levels to inhibit AMPK, which otherwise promotes NFYa phosphorylation and destabilization. NFYa, a transcription factor essential for cardiomyocyte proliferation, has been iden"],"journal":["National science review"],"pagination":["nwaf408"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12796809"],"repository":["biostudies-literature"],"pubmed_title":["PKM1 is required for embryonic cardiomyocyte proliferation through energetic regulation of NFYa stability."],"pmcid":["PMC12796809"],"pubmed_authors":["Liu J","Zhang D","Xu D","Ye W","Wang H","Yang D","Huang R","Zhao Y","Qin S","Su N","Shi G","Kou X","Tang Y","Gao S","Kang L","Wei K"],"additional_accession":[]},"is_claimable":false,"name":"PKM1 is required for embryonic cardiomyocyte proliferation through energetic regulation of NFYa stability.","description":"Pyruvate kinase M1 (PKM1) is a critical enzyme in glycolysis, particularly in high-energy-demand tissues like the heart. However, previous knockout strategies for PKM1 were confounded by compensatory upregulation of its low-activity splice variant, PKM2. Here, we generated a <i>Pkm1</i> mutant mouse model using a point mutation that eliminates PKM1 without compensatory PKM2 upregulation. Homozygous <i>Pkm1</i> mutants exhibited perinatal lethality associated with cardiac dysfunction, characterized by thin myocardium and reduced cardiomyocyte proliferation during mid-to-late gestation. We found that PKM1 sustains ATP levels to inhibit AMPK, which otherwise promotes NFYa phosphorylation and destabilization. NFYa, a transcription factor essential for cardiomyocyte proliferation, has been iden","dates":{"release":"2026-01-01T00:00:00Z","publication":"2026 Jan","modification":"2026-06-03T03:15:04.53Z","creation":"2026-06-03T03:10:39.164Z"},"accession":"S-EPMC12796809","cross_references":{"pubmed":["41536305"],"doi":["10.1093/nsr/nwaf408"]}}