ArticleCell cycle (Georgetown, Tex.)2020
HRD1 prevents atherosclerosis-mediated endothelial cell apoptosis by promoting LOX-1 degradation.
Article in Cell cycle (Georgetown, Tex.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 31 citations in OpenAlex.
- Distinct types of regulated cell death in atherosclerosis.Journal of pharmaceutical analysis · 2026Review
- Ginsenoside Rb1 Targets the HRD1-STING Axis to Mitigate Cholesterol-Induced VSMC Senescence.Journal of clinical laboratory analysis · 2026Article
- Lectin-Like Oxidized Low-Density Lipoprotein Receptor-1 (LOX-1): A Potential Therapeutic Target in Ischemic Stroke.Translational stroke research · 2025Review
- Distinct types of protein modifications in diabetic endothelial dysfunction.Cardiovascular diabetology · 2025Review
- Pharmacological and toxicological roles of Kruppel-like factors (KLFs) in the cardiovascular system: a review.Molecular biology reports · 2025Review
- Endoplasmic reticulum-associated degradation mitigates atherosclerosis by maintaining cellular homeostasis.Frontiers in physiology · 2025Review
- HRD1 reduction promotes cholesterol-induced vascular smooth muscle cell phenotypic change via endoplasmic reticulum stress.Molecular and cellular biochemistry · 2024Article
- Casting Light on the Janus-Faced HMG-CoA Reductase Degradation Protein 1: A Comprehensive Review of Its Dualistic Impact on Apoptosis in Various Diseases.Molecular neurobiology · 2024Review
- Oxidative Stress-Mediated Programmed Cell Death: a Potential Therapy Target for Atherosclerosis.Cardiovascular drugs and therapy · 2024Review
- Ubiquitous regulation of cerebrovascular diseases by ubiquitin-modifying enzymes.Clinical and translational medicine · 2024Review
- USF1 transcriptionally activates USP14 to drive atherosclerosis by promoting EndMT through NLRC5/Smad2/3 axis.Molecular medicine (Cambridge, Mass.) · 2024Article
- New Dawn for Atherosclerosis: Vascular Endothelial Cell Senescence and Death.International journal of molecular sciences · 2023Review
- PTP1B inhibition ameliorates inflammatory injury and dysfunction in ox-LDL-induced HUVECs by activating the AMPK/SIRT1 signaling pathway via negative regulation of KLF2.Experimental and therapeutic medicine · 2022Article
- The Role of KLF2 in the Regulation of Atherosclerosis Development and Potential Use of KLF2-Targeted Therapy.Biomedicines · 2022Review
- HRD1 inhibits fatty acid oxidation and tumorigenesis by ubiquitinating CPT2 in triple-negative breast cancer.Molecular oncology · 2021Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The 3-hydroxy-3-methylglutaryl reductase degradation (HRD1) is an E3 ubiquitin ligase that can preserve heart structure and function, but its role in endothelial dysfunction and atherosclerosis (AS) is unclear. The aim of this study was to explore the role and biological function of HRD1 in AS. HRD1 expression was significantly decreased in atherosclerotic intima and ox-LDL led to a decrease of HRD1 level in endothelial cells (ECs). Forced expression of HRD1 inhibited the endothelial apoptosis induced by ox-LDL. The transcription factor KLF2 specifically bound to the HRD1 promoter and positively regulated HRD1 expression. KLF2 up-regulation could reverse the decrease of HRD1 level in ECs treated with ox-LDL. Further analysis showed that HRD1 interacted with LOX-1 and promoted ubiquitination and degradation of LOX-1 by the proteasome. Deletion of LOX-1 attenuated the ECs apoptosis induced by HRD1 downregulation. Pravastatin, which protected EC from damage via a KLF2-dependent mechanism, could dose-dependently enhanced HRD1 expression in EC exposed to ox-LDL. Interestingly, interference of HRD1 abolished the cytoprotective effect of pravastatin. Collectively, our data indicate that decreased HRD1 expression leads to apoptosis of ECs and restoration of HRD1 expression could represent a novel strategy for human AS therapy.
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