ArticleMolecular biology of the cell2013
Apolipoprotein(a) stimulates nuclear translocation of β-catenin: a novel pathogenic mechanism for lipoprotein(a).
Article in Molecular biology of the cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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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.
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Who cites it
14 citing papers in PubMed, 38 citations in OpenAlex.
- The Roles of Lipoprotein(a) in Atherosclerosis - Minding the Knowledge Gaps.Current atherosclerosis reports · 2026Review
- Metabolic reaction fluxes as amplifiers and buffers of risk alleles for coronary artery disease.Molecular systems biology · 2025Article
- The Lyn/RUVBL1 Complex Promotes Colorectal Cancer Liver Metastasis by Regulating Arachidonic Acid Metabolism Through Chromatin Remodeling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Lipoprotein(a) and cardiovascular disease.The Biochemical journal · 2024Review
- Lipoprotein (a)-Related Inflammatory Imbalance: A Novel Horizon for the Development of Atherosclerosis.Current atherosclerosis reports · 2024Review
- Lipoprotein(a) in Atherosclerotic Diseases: From Pathophysiology to Diagnosis and Treatment.Molecules (Basel, Switzerland) · 2023Review
- Lipoprotein(a) induces caspase-1 activation and IL-1 signaling in human macrophages.Frontiers in cardiovascular medicine · 2023Article
- Lipoprotein(a) and stroke: a two-sample Mendelian randomization study.Frontiers in aging neuroscience · 2023Article
- Long Noncoding RNACirculation · 2021Article
- Association between lipoprotein(a) concentration and the risk of stroke in the Chinese Han population: a retrospective case-control study.Annals of translational medicine · 2020Article
- Oxidized phospholipids as a unifying theory for lipoprotein(a) and cardiovascular disease.Nature reviews. Cardiology · 2019Review
- Follistatin-Like 3 Enhances the Function of Endothelial Cells Derived from Pluripotent Stem Cells by Facilitating β-Catenin Nuclear Translocation Through Inhibition of Glycogen Synthase Kinase-3β Activity.Stem cells (Dayton, Ohio) · 2018Article
- Lipoprotein(a) and its role in inflammation, atherosclerosis and malignancies.Clinical research in cardiology supplements · 2017Article
- Screening for and management of elevated Lp(a).Current cardiology reports · 2013Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lipoprotein(a) (Lp(a)) is associated with cardiovascular disease risk. This may be attributable to the ability of Lp(a) to elicit endothelial dysfunction. We previously reported that apolipoprotein(a) (apo(a); the distinguishing kringle-containing component of Lp(a)) elicits cytoskeletal rearrangements in vascular endothelial cells, resulting in increased cellular permeability. These effects require a strong lysine-binding site (LBS) in apo(a). We now report that apo(a) induces both nuclear β-catenin-mediated cyclooxygenase-2 (COX-2) expression and prostaglandin E2 secretion, indicating a proinflammatory role for Lp(a). Apo(a) caused the disruption of VE-cadherin/β-catenin complexes in a Src-dependent manner, decreased β-catenin phosphorylation, and increased phosphorylation of Akt and glycogen synthase kinase-3β, ultimately resulting in increased nuclear translocation of β-catenin; all of these effects are downstream of apo(a) attenuation of phosphatase and tensin homologue deleted on chromosome 10 activity. The β-catenin-mediated effects of apo(a) on COX-2 expression were absent using a mutant apo(a) lacking the strong LBS. Of interest, the normal and LBS mutant forms of apo(a) bound to human umbilical vein endothelial cells in a similar manner, and the binding of neither was affected by lysine analogues. Taken together, our findings suggest a novel mechanism by which apo(a) can induce proinflammatory and proatherosclerotic effects through modulation of vascular endothelial cell function.
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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.