ArticleNature communications2018
Oxidized phospholipids regulate amino acid metabolism through MTHFD2 to facilitate nucleotide release in endothelial cells.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Reactive oxygen species in thoracic aortic dissection: Insights into mechanisms and disease progression.Redox biology · 2026Review
- MTHFD2: a promising metabolic checkpoint for diseases.Journal of translational medicine · 2026Review
- Investigating the oncogenic potential of MTHFD2 in oral squamous cell carcinoma.Journal of cancer research and clinical oncology · 2026Article
- Endothelial cell metabolism in cardiovascular physiology and disease.Nature reviews. Cardiology · 2025Review
- CYB5R4 sustains endothelial proliferation and ischemia-induced angiogenesis by maintaining RRM2-dependent nucleotide balance.bioRxiv : the preprint server for biology · 2025Article
- Ox-LDL induces a non-inflammatory response enriched for coronary artery disease risk in human endothelial cells.Scientific reports · 2025Article
- Genomic and Transcriptomic Profiling of Amino Acid Compositions in Common Carp Fillets.Animals : an open access journal from MDPI · 2025Article
- Bayesian networks for network inference in biology.Journal of the Royal Society, Interface · 2025Review
- Stimuli-Responsive Nanomedicines for the Treatment of Non-cancer Related Inflammatory Diseases.ACS nano · 2025Review
- Novel Circulating Biomarkers in Aortic Valve Stenosis.International journal of molecular sciences · 2025Review
- Review
- Aiming at early-stage vulnerable plaques: A nanoplatform with dual-mode imaging and lipid-inflammation integrated regulation for atherosclerotic theranostics.Bioactive materials · 2024Article
- Dysregulated cellular metabolism in atherosclerosis: mediators and therapeutic opportunities.Nature metabolism · 2024Review
- Amino Acid Metabolism and Atherosclerotic Cardiovascular Disease.The American journal of pathology · 2024Review
- MTHFD2 in healthy and cancer cells: Canonical and non-canonical functions.npj metabolic health and disease · 2024Review
- New insights in the targets of action of dimethyl fumarate in endothelial cells: effects on energetic metabolism and serine synthesis in vitro and in vivo.Communications biology · 2023Article
- Activation of XBP1 but not ATF6α rescues heart failure induced by persistent ER stress in medaka fish.Life science alliance · 2023Article
- Purinergic signaling during Marek's disease in chickens.Scientific reports · 2023Article
- Proteins Adsorbed during Intraoperative Hemoadsorption and Their In Vitro Effects on Endothelium.Healthcare (Basel, Switzerland) · 2023Article
- Identification of MTHFD2 as a prognostic biomarker and ferroptosis regulator in triple-negative breast cancer.Frontiers in oncology · 2023Article
Corrections and comments
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Authors and funding
32 authors at 10 institutions in 4 countries.
Funding
Abstract
Oxidized phospholipids (oxPAPC) induce endothelial dysfunction and atherosclerosis. Here we show that oxPAPC induce a gene network regulating serine-glycine metabolism with the mitochondrial methylenetetrahydrofolate dehydrogenase/cyclohydrolase (MTHFD2) as a causal regulator using integrative network modeling and Bayesian network analysis in human aortic endothelial cells. The cluster is activated in human plaque material and by atherogenic lipoproteins isolated from plasma of patients with coronary artery disease (CAD). Single nucleotide polymorphisms (SNPs) within the MTHFD2-controlled cluster associate with CAD. The MTHFD2-controlled cluster redirects metabolism to glycine synthesis to replenish purine nucleotides. Since endothelial cells secrete purines in response to oxPAPC, the MTHFD2-controlled response maintains endothelial ATP. Accordingly, MTHFD2-dependent glycine synthesis is a prerequisite for angiogenesis. Thus, we propose that endothelial cells undergo MTHFD2-mediated reprogramming toward serine-glycine and mitochondrial one-carbon metabolism to compensate for the loss of ATP in response to oxPAPC during atherosclerosis.
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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.