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Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Visium]

ABSTRACT: Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Visium]

PROVIDER: PRJNA974494 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24673361.fastq.gz	Fastqsanger.gz
	SRR24673362.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Visium]

Project description:Cardiomyocytes are highly metabolic cells responsible for generating the contractile force that drives heart function. During fetal development and regeneration, these cells undergo active division but lose their proliferation activity in the adult heart. The mechanisms that coordinate their metabolism and proliferation are not fully understood. Here, we study the developmental functions of the transcription factor NFYa, which we previously identified from regenerating cardiomyocytes. We show that loss of NFYa profoundly alters cardiomyocyte composition, with a decrease in immature regenerative cells and an increase in trabecular and mature cardiomyocytes, as revealed by spatial and single-cell transcriptome analyses. NFYa-deleted cardiomyocytes exhibited reduced proliferation and impaired mitochondrial metabolism, contributing to the cardiac growth defect. NFYa acts as a transcriptional activator of mitochondrial metabolic genes as well as cell-cycle genes in cardiomyocytes through its interaction with the cofactor SP2, providing a direct link between metabolism and proliferation at the gene transcriptional level. Our study reveals a key role of NFYa in regulating cardiac growth before birth and a previously unrecognized transcriptional control mechanism of metabolic genes in the heart, and highlights the importance of mitochondrial metabolism during fetal heart development and regeneration.

2023-10-13 | GSE232962 | GEO

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Multiome]

2023-10-13 | GSE232961 | GEO

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [ChIP-seq]

2023-10-13 | GSE232960 | GEO

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development

Project description:Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development

| PRJNA974492 | ENA

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Multiome]

Project description:Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Multiome]

| PRJNA974493 | ENA

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [ChIP-seq]

Project description:Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [ChIP-seq]

| PRJNA974488 | ENA

Pkm1 is required for embryonic cardiomyocyte proliferation through energetic regulation of NFYa stability

Project description:Pyruvate Kinase M1 (PKM1) is a critical enzyme in energy metabolism, 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 Pkm1 mutant mouse model using a point mutation that deletes Pkm1 without elevating PKM2. Homozygous Pkm1 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, is identified as a key mediator linking metabolic status to cell cycle activity. These findings identify the PKM1-AMPK-NFYa axis in energetic regulation of cardiomyocyte proliferation in embryonic heart, offering new insights into the function of PKM1 and the broader impact of energy metabolism on cardiac development, while also shedding light on the potential metabolic underpinnings of congenital heart diseases.

2026-01-21 | GSE290043 | GEO

Pkm1 is required for embryonic cardiomyocyte proliferation through energetic regulation of NFYa stability

Project description:Pkm1 is required for embryonic cardiomyocyte proliferation through energetic regulation of NFYa stability

| PRJNA1226090 | ENA

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-10-13 | GSE232963 | GEO

Gas6 promotes Cardiomyocyte Proliferation and Heart Regeneration

Project description:Ischemic heart disease remains a leading cause of mortality, with limited adult cardiac regeneration due to insufficient cardiomyocyte proliferation. This study investigates the role of Growth Arrest-Specific Gene 6 (Gas6) in regulating cardiomyocyte cell cycle and promoting cardiac repair. Gas6 expression declines postnatally in cardiomyocytes but increases during neonatal heart regeneration following myocardial infarction (MI). Cardiomyocyte-specific Gas6 knockout (Gas6CKO) mice exhibited reduced cardiomyocyte proliferation, decreased total cardiomyocyte numbers, and delayed-onset heart failure with ventricular dilation by ~250 days, as confirmed by transcriptomic analysis revealing downregulation of cell cycle pathways and upregulation of fibrotic and contractile genes in Gas6CKO versus control hearts at 250 days. Conversely, AAV9-mediated cardiomyocyte-specific Gas6 overexpression enhanced neonatal cardiomyocyte proliferation, dedifferentiation, and hyperplastic growth, while in adult MI models, it improved cardiac function, reduced infarct size, and increased proliferative markers (Ki67, pH3, Aurora B) in the border zone. Bulk RNA-sequencing of primary mouse cardiomyocytes overexpressing Ad-Gas6 versus controls identified upregulated cell cycle and mitotic pathways, alongside downregulated cardiac contraction and extracellular matrix organization, with transcription factor enrichment highlighting Yap-mediated activation via TEAD2 and E2F1. Mechanistically, Gas6 binds Sav1 to disrupt the Sav1-Mst1 complex, inhibiting Hippo pathway phosphorylation, promoting Yap nuclear translocation, and driving cell cycle gene expression. These findings position Gas6 as a therapeutic target for cardiac regeneration in ischemic heart disease.

2026-08-21 | GSE306068 | GEO

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