ArticleEMBO reports2021
Fatty acid oxidation is required for embryonic stem cell survival during metabolic stress.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 33 citations in OpenAlex.
- Metabolic oxidoreductases: central regulators of the epigenetic landscapes in stemness.Experimental & molecular medicine · 2026Review
- Transcriptomic analysis identifies FABP5 as a candidate regulator of lipid accumulation in metabolic dysfunction-associated fatty liver disease.Frontiers in endocrinology · 2026Article
- Microprotein PLUM encoded by Lin28b uORF is a cytoplasmic determinant of pluripotency and embryonic development.Nature communications · 2025Article
- Tfcp2l1 as a central integrator of hypoxia, dedifferentiation, and tumor progression.Journal of experimental & clinical cancer research : CR · 2025Review
- CPT1A/HIF-1α positive feedback loop induced fatty acid oxidation metabolic pathway contributes to the L-ascorbic acid-driven angiogenesis in breast cancer.Breast cancer research : BCR · 2025Article
- The protective role of GPX4 in naïve ESCs is highlighted by induced ferroptosis resistance through GPX4 expression.Redox biology · 2025Article
- Crosstalk between Signaling Pathways and Energy Metabolism in Pluripotency.International journal of stem cells · 2025Review
- Intestinal DHA-PA-PG axis promotes digestive organ expansion by mediating usage of maternally deposited yolk lipids.Nature communications · 2024Article
- Cpt1a Drives primed-to-naïve pluripotency transition through lipid remodeling.Communications biology · 2024Article
- The role of lipids in genome integrity and pluripotency.Biochemical Society transactions · 2024Review
- Selective Elimination of Genetic Variants of Human Embryonic Stem Cells from High Vulnerability to Ferroptosis.Biomaterials research · 2024Article
- Beyond energy and growth: the role of metabolism in developmental signaling, cell behavior and diapause.Development (Cambridge, England) · 2023Article
- SOX9 is a key component of RUNX2-regulated transcriptional circuitry in osteosarcoma.Cell & bioscience · 2023Article
- Ablation of ZC3H11A causes early embryonic lethality and dysregulation of metabolic processes.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- CPT1C-mediated fatty acid oxidation facilitates colorectal cancer cell proliferation and metastasis.Acta biochimica et biophysica Sinica · 2023Article
- Dysregulation of Mitochondrial Translation Caused by CBFB Deficiency Cooperates with Mutant PIK3CA and Is a Vulnerability in Breast Cancer.Cancer research · 2023Article
- Requirement for STAT3 and its target, TFCP2L1, in self-renewal of naïve pluripotent stem cells in vivo and in vitro.Biology open · 2023Article
- Review
- Early Life Stress and Metabolic Plasticity of Brain Cells: Impact on Neurogenesis and Angiogenesis.Biomedicines · 2021Review
- Fatty acid oxidation is required for embryonic stem cell survival during metabolic stress.EMBO reports · 2021Article
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 2 countries.
Funding
Abstract
Metabolic regulation is critical for the maintenance of pluripotency and the survival of embryonic stem cells (ESCs). The transcription factor Tfcp2l1 has emerged as a key factor for the naïve pluripotency of ESCs. Here, we report an unexpected role of Tfcp2l1 in metabolic regulation in ESCs-promoting the survival of ESCs through regulating fatty acid oxidation (FAO) under metabolic stress. Tfcp2l1 directly activates many metabolic genes in ESCs. Deletion of Tfcp2l1 leads to an FAO defect associated with upregulation of glucose uptake, the TCA cycle, and glutamine catabolism. Mechanistically, Tfcp2l1 activates FAO by inducing Cpt1a, a rate-limiting enzyme transporting free fatty acids into the mitochondria. ESCs with defective FAO are sensitive to cell death induced by glycolysis inhibition and glutamine deprivation. Moreover, the Tfcp2l1-Cpt1a-FAO axis promotes the survival of quiescent ESCs and diapause-like blastocysts induced by mTOR inhibition. Thus, our results reveal how ESCs orchestrate pluripotent and metabolic programs to ensure their survival in response to metabolic stress.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.