ArticleCirculation research2022
L-2-Hydroxyglutarate Protects Against Cardiac Injury via Metabolic Remodeling.
Article in Circulation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 35 citations in OpenAlex.
- Interplay between ischemia-reperfusion and metabolic reprogramming.Apoptosis : an international journal on programmed cell death · 2026Review
- ExplainBind: Explainable Physicochemical Determinants of Protein-Ligand Binding via Non-Covalent Interactions.bioRxiv : the preprint server for biology · 2026Article
- The Role of the Pentose Phosphate Pathway in Cardiovascular Diseases.Cardiovascular drugs and therapy · 2026Review
- Loss of calcium-dependent phospholipase A2 contributes to multi-omic changes in mouse denervated skeletal muscle.Physiological reports · 2026Article
- Circulating Extracellular Vesicles in the Pathogenesis of Heart Failure in Patients With Chronic Kidney Disease.Circulation · 2026Article
- Nucleophosmin 1 lactylation in graft kidney induces ferroptotic trigger waves that exacerbate delayed graft function.Nature communications · 2025Article
- Irisin regulates cardiac myocyte energy metabolic remodeling involved the ADRA1A-AMPK signaling pathwayng pathway.European journal of medical research · 2025Article
- D2HGDH Deficiency Regulates Seizures through GSH/Prdx6/ROS-Mediated Excitatory Synaptic Activity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Branched-chain α-ketoacids aerobically activate HIF1α signalling in vascular cells.Nature metabolism · 2024Article
- Metabolic Responses to Redox Stress in Vascular Cells.Antioxidants & redox signaling · 2024Review
- Isolated Perfused Hearts for Cardiovascular Research: An Old Dog with New Tricks.Journal of cardiovascular translational research · 2024Review
- Branched chain α-ketoacids aerobically activate HIF1α signaling in vascular cells.bioRxiv : the preprint server for biology · 2024Article
- Pharmacological Effects of Botanical Drugs on Myocardial Metabolism in Chronic Heart Failure.Chinese journal of integrative medicine · 2024Review
- Hypoxic adaptation of mitochondria and its impact on tumor cell function.Seminars in cancer biology · 2024Review
- Cardiovascular aging: spotlight on mitochondria.American journal of physiology. Heart and circulatory physiology · 2024Review
- Review
- Insulin-induced gene 2 protects against hepatic ischemia-reperfusion injury via metabolic remodeling.Journal of translational medicine · 2023Article
- Cardiac macrophages and emerging roles for their metabolism after myocardial infarction.The Journal of clinical investigation · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
backgroundL-2-hydroxyglutarate (L2HG) couples mitochondrial and cytoplasmic energy metabolism to support cellular redox homeostasis. Under oxygen-limiting conditions, mammalian cells generate L2HG to counteract the adverse effects of reductive stress induced by hypoxia. Very little is known, however, about whether and how L2HG provides tissue protection from redox stress during low-flow ischemia (LFI) and ischemia-reperfusion injury. We examined the cardioprotective effects of L2HG accumulation against LFI and ischemia-reperfusion injury and its underlying mechanism using genetic mouse models. METHODS AND
resultsL2HG accumulation was induced by homozygous (L2HGDH [L-2-hydroxyglutarate dehydrogenase]
conclusionL2HGDH deletion-induced L2HG accumulation protects against myocardial injury during LFI and ischemia-reperfusion through a metabolic shift of glucose flux from glycolysis towards the pentose phosphate pathway. L2HG offers a novel mechanism for eliminating reactive oxygen species from myocardial tissue, mitigating redox stress, reducing myocardial infarct size, and preserving high-energy phosphates and cardiac function. Targeting L2HG levels through L2HGDH activity may serve as a new therapeutic strategy for cardiovascular diseases related to oxidative injury.
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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.