ArticleFrontiers in pharmacology2021
C1q/TNF-Related Protein 9 Attenuates Atherosclerosis by Inhibiting Hyperglycemia-Induced Endothelial Cell Senescence Through the AMPKα/KLF4 Signaling Pathway.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Organokines in COVID-19: A Systematic Review.Cells · 2023Pooled it
- Cellular and Molecular Mechanisms of Hyperglycemia-Induced Atherosclerosis and Intervention Strategies of Chinese Herbal Medicine.Drug design, development and therapy · 2026Review
- Traditional Chinese medicine in diabetes management: a comprehensive review of mechanisms and therapeutic potential.Frontiers in endocrinology · 2026Review
- The mechanism of C1q/TNF-related proteins (CTRPs) in atherosclerosis associated with type 2 diabetes mellitus.European journal of medical research · 2025Review
- Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Mechanisms of endothelial senescence and vascular aging.Biogerontology · 2025Review
- N-terminal domain of CTRP9 promotes cardiac fibroblast activation in myocardial infarction via Rap1/Mek/Erk pathway.Journal of translational medicine · 2025Article
- The Therapeutic Effect and Mechanism of Traditional Chinese Medicine in Type 2 Diabetes Mellitus and Its Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2025Review
- MicroRNA-34a Mediates the Aldosterone-Induced Acceleration of Endothelial Senescence.International journal of hypertension · 2025Article
- Mesenchymal stem cell-derived extracellular vesicles relieve endothelial cell senescence via recovering CTRP9 upon repressing miR-674-5p in atherosclerosis.Regenerative therapy · 2024Article
- Cellular Senescence: A Bridge Between Diabetes and Microangiopathy.Biomolecules · 2024Review
- Quercetin Attenuates KLF4-Mediated Phenotypic Switch of VSMCs to Macrophage-like Cells in Atherosclerosis: A Critical Role for the JAK2/STAT3 Pathway.International journal of molecular sciences · 2024Article
- Article
- Diabetes Mellitus to Accelerated Atherosclerosis: Shared Cellular and Molecular Mechanisms in Glucose and Lipid Metabolism.Journal of cardiovascular translational research · 2024Review
- CTRP13 Mitigates Endothelial Cell Ferroptosis via the AMPK/KLF4 Pathway: Implications for Atherosclerosis Protection.Medical science monitor : international medical journal of experimental and clinical research · 2024Article
- Treatment of advanced atherosclerotic mice with ABT-263 reduced indices of plaque stability and increased mortality.JCI insight · 2024Article
- Multifaced roles of adipokines in endothelial cell function.Frontiers in endocrinology · 2024Review
- Traditional Chinese medicine and its active substances reduce vascular injury in diabetes via regulating autophagic activity.Frontiers in pharmacology · 2024Review
- Hypermethylation of the CTRP9 promoter region promotes Hcy induced VSMC lipid deposition and foam cell formation via negatively regulating ER stress.Scientific reports · 2023Article
- PPARγ in Atherosclerotic Endothelial Dysfunction: Regulatory Compounds and PTMs.International journal of molecular sciences · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperglycemia-induced endothelial cell senescence has been widely reported to be involved in the pathogenesis of type 2 diabetes mellitus‒accelerated atherosclerosis. Thus, understanding the underlying mechanisms and identifying potential therapeutic targets for endothelial cell senescence are valuable for attenuating atherosclerosis progression. C1q/tumor necrosis factor-related protein 9 (CTRP9), an emerging potential cardiokine, exerts a significant protective effect with respect to atherosclerosis, particularly in endothelial cells. However, the exact mechanism by which CTRP9 prevents endothelial cells from hyperglycemia-induced senescence remains unclear. This study aimed to investigate the effects of CTRP9 on hyperglycemia-induced endothelial cell senescence and atherosclerotic plaque formation in diabetic apolipoprotein E knockout (ApoE KO) mice. Human umbilical vein endothelial cells (HUVECs) were cultured in normal glucose (5.5 mM) and high glucose (40 mM) with or without recombinant human CTRP9 protein (3 μg/ml) for 48 h. Purified lentiviruses overexpressing CTRP9 (Lv-CTRP9) and control vectors containing green fluorescent protein (Lv-GFP) were injected via the tail vein into streptozotocin-induced diabetic ApoE KO mice. Results revealed that exposure of HUVECs to HG significantly increased the expression of Krüppel-like factor 4 (KLF4) and cyclin-dependent kinase inhibitor p21 (p21) and decreased that of telomerase reverse transcriptase (TERT). Treatment with recombinant human CTRP9 protein protected HUVECs from HG-induced premature senescence and dysfunction. CTRP9 promoted the phosphorylation of AMP-activated kinase (AMPK), attenuated the expression of KLF4 and p21 induced by HG, and increased the expression of TERT in HUVECs. Furthermore, in the background of AMPKα knockdown or KLF4 activation, the protective effects of CTRP9 were abolished.
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