ArticleInflammation2019
CTRP3 Alleviates Ox-LDL-Induced Inflammatory Response and Endothelial Dysfunction in Mouse Aortic Endothelial Cells by Activating the PI3K/Akt/eNOS Pathway.
Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 62 citations in OpenAlex.
- Multifunctional Roles and Therapeutic Prospects of C1q/TNF-Related Protein 3 (CTRP3) in Human Diseases.Current medical science · 2025Review
- Unveiling the roles of CTRP family in cardiac remodeling.Journal of molecular medicine (Berlin, Germany) · 2025Review
- Effect of Bazi Bushen Capsule on D-Galactose-Induced Human Endothelial Cell Senescence Through PI3K/Akt/eNOS Signaling Pathway.Aging medicine (Milton (N.S.W)) · 2025Article
- Network pharmacology analysis and experimental validation elucidate the protective mechanisms of BYHWD against hypoxia/reoxygenation-induced endothelial cell injury.Frontiers in medicine · 2025Article
- Impact and Mechanisms of Action of BDNF on Neurological Disorders, Cancer, and Cardiovascular Diseases.CNS neuroscience & therapeutics · 2024Review
- Article
- Decreased circulating CTRP3 levels in acute and chronic cardiovascular patients.Journal of molecular medicine (Berlin, Germany) · 2024Article
- Ethanol extract ofBiomedical reports · 2024Article
- Expression of insulin-like growth factor binding protein-3 in HELLP syndrome.BMC pregnancy and childbirth · 2023Article
- CTRP family in diseases associated with inflammation and metabolism: molecular mechanisms and clinical implication.Acta pharmacologica Sinica · 2023Review
- Complement 1q/Tumor Necrosis Factor-Related Proteins (CTRPs): Structure, Receptors and Signaling.Biomedicines · 2023Review
- Multi-faceted roles of C1q/TNF-related proteins family in atherosclerosis.Frontiers in immunology · 2023Review
- Adipokines in atherosclerosis: unraveling complex roles.Frontiers in cardiovascular medicine · 2023Review
- Research Progress and Molecular Mechanisms of Endothelial Cells Inflammation in Vascular-Related Diseases.Journal of inflammation research · 2023Review
- The role of epicardial adipose tissue dysfunction in cardiovascular diseases: an overview of pathophysiology, evaluation, and management.Frontiers in endocrinology · 2023Review
- Exogenous Hydrogen Sulfide Activates PI3K/Akt/eNOS Pathway to Improve Replicative Senescence in Human Umbilical Vein Endothelial Cells.Cardiology research and practice · 2023Article
- Astragaloside IV Regulates Insulin Resistance and Inflammatory Response of Adipocytes via Modulating CTRP3 and PI3K/AKT Signaling.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2022Article
- Decreased EpicardialInternational journal of molecular sciences · 2022Article
- A κ-OR Agonist Protects the Endothelial Function Impaired by Hyperuricemia Through Regulating the Akt/eNOS Signal Pathway.Probiotics and antimicrobial proteins · 2022Article
- Administration of rTMS Alleviates Stroke-Induced Cognitive Deficits by Modulating miR-409-3p/CTRP3/AMPK/Sirt1 Axis.Journal of molecular neuroscience : MN · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C1q/tumor necrosis factor-related protein-3 (CTRP3) is a novel, certified, adipokine that beneficially regulates metabolism and inflammation in the cardiovascular system. Atherosclerotic plaque rupturing and secondary thrombosis cause vascular disorders, such as myocardial infarction and unstable angina. However, the underlying role of CTRP3 in atherosclerosis remains unclear. In this study, we aimed to elucidate whether and how CTRP3 ameliorates inflammation and endothelial dysfunction caused by oxidized low-density lipoprotein (ox-LDL). We first confirmed that CTRP3 expression was inhibited in ApoE-/- mice, compared to normal mice. Then, pcDNA-CTRP3 and siCTRP3 were transfected into mouse aortic endothelial cells after ox-LDL stimulation, and we observed that enhanced CTRP3 remarkably downregulated CRP, TNF-α, IL-6, CD40, and CD40L. We also observed that overexpression of CTRP3 elevated cell activity and decreased lactated hydrogenase release, accompanied by a marked reduction in cell apoptosis induced by ox-LDL. Meanwhile, overexpressed CTRP3 caused a decrease in Ang II, ICAM-1, and VCAM-1 expression, and it restored the balance between ET-1 and NO. Mechanism analysis confirmed that incremental CTRP3 upregulated p-PI3K, p-Akt, and p-eNOS expression, indicating that CTRP3 facilitated activation of the PI3K/Akt/eNOS pathway. On the contrary, siCTRP3 exerted the opposite effect to this activation. Blocking these pathways using LY294002 or L-NAME attenuated the protective role of CTRP3. Overall, these results suggest that CTRP3 can efficiently inhibit the inflammatory response and endothelial dysfunction induced by ox-LDL in mouse aortic endothelial cells, perhaps by activating the PI3K/Akt/eNOS pathway, indicating a promising strategy against atherosclerosis.
Indexed as
Identifiers
What OpenQuestion holds
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.