ReviewArteriosclerosis, thrombosis, and vascular biology2023
Quartet of APOCs and the Different Roles They Play in Diabetes.
Review in Arteriosclerosis, thrombosis, and vascular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 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
25 citing papers in PubMed, 33 citations in OpenAlex.
- Early Hepatic Transcriptomic Responses to High-Fat Diet in Apolipoprotein A-IV Knockout Mice.Metabolites · 2026Article
- Proteomic analysis of plasma and extracellular vesicles from subjects with impaired vascular health.Bioscience reports · 2026Article
- Exploratory LC-MS/MS-Based Proteomic and Lipidomic Profiling of Plasma Samples from Premature Coronary Artery Disease Patients: A Pilot Study in a South Asian Population.International journal of molecular sciences · 2026Article
- Kidney-Vascular Metabolic Crosstalk: Altered Lipoproteins in CKD.Circulation research · 2026Review
- Proteomics profiling of serum and liver in GSD Ia and Ib patients: insights into complication mechanisms and circulation biomarkers.Journal of translational medicine · 2026Article
- Sex-specific cardioprotective role of miR-30a-5p through estrogen-dependent mechanisms in a mouse model of heart failure.Cardiovascular diabetology · 2026Article
- HDL metabolism and function in diabetes mellitus.Nature reviews. Endocrinology · 2026Review
- Decoding the triglyceride-glucose index in metabolic dysfunction-associated steatotic liver disease: integrative insights from Mendelian randomization, cross-tissue transcriptomics, and spatial multi-omics.International journal of surgery (London, England) · 2026Article
- A Robust Serum Proteomic Signature of the E2 Allele of Apolipoprotein E.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Clinical Relevance and Utility of Serum APOC2 Levels in Patients with Type 2 Diabetes Mellitus: A Comparative Study on Subjects with and without Pyogenic Liver Abscess.Hepatic medicine : evidence and research · 2026Article
- Proteome Profiling of Rabies-Infected and Uninfected Dog Brain Tissues, Cerebrospinal Fluids and Serum Samples.Proteomes · 2025Article
- Quantifying interventional causality by knockoff operation.Science advances · 2025Article
- Shared genetics of lung cancer and type 2 diabetes: a large-scale genome-wide cross-trait analysis.Translational lung cancer research · 2025Article
- Dietary Intake of a Milk Sphingolipid-Rich MFGM/EV Concentrate Ameliorates Age-Related Metabolic Dysfunction.Nutrients · 2025Article
- The proteome of circulating extracellular vesicles and their functional effect on platelets vary with the isolation method.Scientific reports · 2025Article
- Sudden Cardiac Death in Pregnant Women-Literature Review and Autopsy Findings.Diagnostics (Basel, Switzerland) · 2025Review
- Molecular Regulation and Therapeutic Targeting of VLDL Production in Cardiometabolic Disease.Cellular and molecular gastroenterology and hepatology · 2025Review
- ANGPTL3 and residual atherosclerotic risk: from lipid metabolism to therapeutic targeting.Frontiers in endocrinology · 2025Review
- Proteomic and Lipidomic Plasma Evaluations Reveal Biomarkers for Domoic Acid Toxicosis in California Sea Lions.Journal of proteome research · 2024Article
- Multifaceted Role of Apolipoprotein C3 in Cardiovascular Disease Risk and Metabolic Disorder in Diabetes.International journal of molecular sciences · 2024Review
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 1 institution in 1 country.
Funding
Abstract
APOA1 and APOB are the structural proteins of high-density lipoprotein and APOB-containing lipoproteins, such as low-density lipoprotein and very low-density lipoprotein, respectively. The 4 smaller APOCs (APOC1, APOC2, APOC3, and APOC4) are exchangeable apolipoproteins; they are readily transferred among high-density lipoproteins and APOB-containing lipoproteins. The APOCs regulate plasma triglyceride and cholesterol levels by modulating substrate availability and activities of enzymes interacting with lipoproteins and by interfering with APOB-containing lipoprotein uptake through hepatic receptors. Of the 4 APOCs, APOC3 has been best studied in relation to diabetes. Elevated serum APOC3 levels predict incident cardiovascular disease and progression of kidney disease in people with type 1 diabetes. Insulin suppresses APOC3 levels, and accordingly, elevated APOC3 levels associate with insulin deficiency and insulin resistance. Mechanistic studies in a mouse model of type 1 diabetes have demonstrated that APOC3 acts in the causal pathway of diabetes-accelerated atherosclerosis. The mechanism is likely due to the ability of APOC3 to slow the clearance of triglyceride-rich lipoproteins and their remnants, thereby causing an increased accumulation of atherogenic lipoprotein remnants in lesions of atherosclerosis. Less is known about the roles of APOC1, APOC2, and APOC4 in diabetes.
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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.