ReviewNature reviews. Cardiology2025
Apolipoprotein B-containing lipoproteins in atherogenesis.
Review in Nature reviews. Cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
What it found
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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
42 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Review
- Lichen-Derived Bioactive Compounds in Diabetes and Cardiovascular Risk: Experimental Evidence, Mechanisms, and Translational Challenges.Biomedicines · 2026Review
- Divergent biological consequences of APOE isoforms across industrialized and non-industrial environments.PLoS genetics · 2026Article
- Congenital Hypothyroidism and Atherosclerosis: An Endocrine Model of Early-Life Cardiovascular Risk.Journal of cardiovascular development and disease · 2026Review
- Linking Lipidomics to Vulnerable Coronary Plaques: A PROSPECT II Substudy.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Risk-weighted apoB: a novel summary metric outperforming traditional lipid biomarkers in predicting coronary heart disease.European heart journal · 2026Article
- Metabolic syndrome is associated with accelerated brain aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Residual cardiovascular risk in coronary artery disease: from pathophysiology to established and novel therapies.Nature reviews. Cardiology · 2026Review
- Age-related metabolomic signatures and stroke susceptibility in a population-based cohort.GeroScience · 2026Article
- Genetic Determinants of Severe Hypertriglyceridemia: Rare Variants inInternational journal of molecular sciences · 2026Article
- Variable selection-combined causal mediation analysis for continuous treatments with application to large-dimensional biomedical data.PLoS computational biology · 2026Article
- Increased transvascular retention of atherogenic lipoproteins in type 2 diabetes relates to their enhanced proteoglycan binding.JCI insight · 2026Article
- Metal-Organic Framework as Contrast Agents for Magnetic Resonance Imaging.Pharmaceutics · 2026Review
- Article
- From lipoprotein metabolism to blood clotting: Highlights of the 2025 Fredrickson lipid research conference.Journal of lipid research · 2026Article
- Exogenous Ganglioside GM3 Attenuates Atherosclerosis via Multi-Organ Modulation of Lipid Metabolism.Pharmaceutics · 2026Article
- Rosmarinic Acid Targets AKR1B1 to Ameliorate Atherosclerosis via Vascular Endothelial Cell Energy Metabolism Regulation.Biomolecules · 2026Article
- A population-based study of the sex-specific associations between apolipoprotein B and incidence of atrial fibrillation.Lipids in health and disease · 2026Article
- Apolipoprotein C-III: Risk-factor, Regulator of Triglyceride-rich Lipoprotein Metabolism and Therapeutic Target.Current atherosclerosis reports · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apolipoprotein B (apoB) is the main structural protein of LDLs, triglyceride-rich lipoproteins and lipoprotein(a), and is crucial for their formation, metabolism and atherogenic properties. In this Review, we present insights into the role of apoB-containing lipoproteins in atherogenesis, with an emphasis on the mechanisms leading to plaque initiation and growth. LDL, the most abundant cholesterol-rich lipoprotein in plasma, is causally linked to atherosclerosis. LDL enters the artery wall by transcytosis and, in vulnerable regions, is retained in the subendothelial space by binding to proteoglycans via specific sites on apoB. A maladaptive response ensues. This response involves modification of LDL particles, which promotes LDL retention and the release of bioactive lipid products that trigger inflammatory responses in vascular cells, as well as adaptive immune responses. Resident and recruited macrophages take up modified LDL, leading to foam cell formation and ultimately cell death due to inadequate cellular lipid handling. Accumulation of dead cells and cholesterol crystallization are hallmarks of the necrotic core of atherosclerotic plaques. Other apoB-containing lipoproteins, although less abundant, have substantially greater atherogenicity per particle than LDL. These lipoproteins probably contribute to atherogenesis in a similar way to LDL but might also induce additional pathogenic mechanisms. Several targets for intervention to reduce the rate of atherosclerotic lesion initiation and progression have now been identified, including lowering plasma lipoprotein levels and modulating the maladaptive responses in the artery wall.
Indexed as
Identifiers
39743565What 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.