ArticleCell stress & chaperones2018
NR4A1 contributes to high-fat associated endothelial dysfunction by promoting CaMKII-Parkin-mitophagy pathways.
Article in Cell stress & chaperones, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 73 citations in OpenAlex.
- Disrupted Mitochondrial Quality Control in Atherosclerotic Disease: Mitophagy and Dynamics in Focus.JACC. Basic to translational science · 2026Review
- Calcium and TRPML-Mediated Autophagy: Implications in Cancer, Cardiovascular Diseases, and Cardio-Oncology.Cardiovascular toxicology · 2026Review
- LDL oxidation and cerebrovascular aging: mechanisms of endothelial dysfunction, inflammation, and vascular cognitive impairment and dementia.Redox biology · 2026Review
- NPC1L1, stabilized by PABPC1/IGF2BP1, accelerates atherosclerosis by enhancing CYP11A1-mediated mitophagy and ferroptosis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Endothelial mitochondrial homeostasis in the development and progression of atherosclerosis.Frontiers in cardiovascular medicine · 2026Review
- Orphan Nuclear Receptor NR4A1 Promotes Proliferation and Osteogenic Differentiation of Valvular Interstitial Cells through Activation of CCND2.International journal of biological sciences · 2026Article
- Targeting autophagy to enhance cancer immunotherapy: emerging mechanisms and strategies.Medical oncology (Northwood, London, England) · 2025Review
- A narrative review on bridging the gap between periodontitis and cardiovascular disease: exploring the cellular and molecular mechanisms of periodontitis-driven atherosclerosis.Molecular biology reports · 2025Review
- Endothelial major vault protein alleviates vascular remodeling via promoting Parkin-mediated mitophagy.Nature communications · 2025Article
- Syntaxin 17 Translocation Mediated Mitophagy Switching Drives Hyperglycemia-Induced Vascular Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- NR4A1 Acts as a Novel Regulator of Platelet Activation and Thrombus Formation.Circulation research · 2025Article
- The Role of Endothelial Cell Mitophagy in Age-Related Cardiovascular Diseases.Aging and disease · 2024Review
- Semaglutide ameliorates cardiac remodeling in male mice by optimizing energy substrate utilization through the Creb5/NR4a1 axis.Nature communications · 2024Article
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- Role of PTEN-Induced Protein Kinase 1 as a Mitochondrial Dysfunction Regulator in Cardiovascular Disease Pathogenesis.Vascular specialist international · 2024Review
- Astaxanthin Inhibits HMarine drugs · 2024Article
- The role of mitochondrial dynamics in disease.MedComm · 2023Review
- Mapping cardiac remodeling in chronic kidney disease.Science advances · 2023Article
- Z-ligustilide preferentially caused mitochondrial dysfunction in AML HL-60 cells by activating nuclear receptors NUR77 and NOR1.Chinese medicine · 2023Article
- Mitochondrial Dysfunction in the Cardio-Renal Axis.International journal of molecular sciences · 2023Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkin-related mitophagy is vital for endothelial cell viability and the development of atherosclerosis, although the upstream regulatory factor underlying Parkin-mediated mitophagy in endothelial apoptosis and atherosclerosis progression remains unknown. In the present study, we demonstrated that nuclear receptor subfamily 4 group A member 1 (NR4A1) is actually expressed in aortic endothelial cells (AECs) under oxidized low-density lipoprotein (ox-LDL) treatment in vitro or isolated from high-fat treated mice in vivo. Higher NR4A1 levels were associated with AEC apoptosis, mitochondrial dysfunction, and energy disorder. At the molecular level, ox-LDL stimulation increased NR4A1 expression, which evoked Parkin-mediated mitophagy. Excessive mitophagy overtly consumed mitochondrial mass, leading to an energy shortage and mitochondrial dysfunction. However, loss of NR4A1 protected AECs against ox-LDL induced apoptosis by inhibiting excessive mitophagy. Furthermore, we also identified that NR4A1 regulated Parkin activation via post-transcriptional modification by Ca2
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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.