ReviewMolecular medicine (Cambridge, Mass.)2012
The interaction of ApoA-I and ABCA1 triggers signal transduction pathways to mediate efflux of cellular lipids.
Review in Molecular medicine (Cambridge, Mass.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 114 citations in OpenAlex.
- Association of Circulating Apolipoprotein AI Levels in Patients With Alzheimer's Disease: A Systematic Review and Meta-Analysis.Frontiers in aging neuroscience · 2022Pooled it
- Molecular Dynamics Simulations Reveal Structural Changes Associated with the ABCA1 R230C Functional Variant.International journal of molecular sciences · 2026Article
- PFAS Exposure and Metabolic Disorders: Mechanistic Insights into Lipid and Glucose Homeostasis.Biomolecules · 2026Review
- ABCA1-mediated lipid efflux restrains oxidative stress and neuroinflammation after spinal cord injury.Journal of neuroinflammation · 2026Article
- The Structural and Functional Journey of Apolipoprotein A-I Through the Human Body.Current atherosclerosis reports · 2026Review
- Inventive HDL Mimicking Nanoparticles: A Promising Frontier in Cardiovascular Disease Management.Cardiovascular toxicology · 2025Review
- Effects of HDL Structure and Function in Peripheral Artery Disease.Biomolecules · 2025Article
- An intermediate activation state primes Langerhans cell migration from the epidermis.bioRxiv : the preprint server for biology · 2025Article
- Spatiotemporal analysis of Crohn's disease reveals PECAM2 signaling at the basis of the inflammation-to-fibrosis transition.Journal of Crohn's & colitis · 2025Article
- Apolipoprotein A (ApoA) in Neurological Disorders: Connections and Insights.International journal of molecular sciences · 2025Review
- Treatment Resistant Persister Cells Exploit Macrophage Lipid Metabolism to Sustain Glioblastoma Growth.bioRxiv : the preprint server for biology · 2025Article
- Differential proteomic profiles between cognitive frail and robust older adults from the MELoR cohort.GeroScience · 2025Article
- Article
- Hormone correction of dysfunctional metabolic gene expression in stem cell-derived liver tissue.Stem cell research & therapy · 2025Article
- Article
- Engineered model of heart tissue repair for exploring fibrotic processes and therapeutic interventions.Nature communications · 2024Article
- LncRNA DANCR promotes macrophage lipid accumulation through modulation of membrane cholesterol transporters.Aging · 2024Article
- Article
- Review
- Etiology of lipid-laden macrophages in the lung.International immunopharmacology · 2023Review
3 more citing papers are in PubMed but not listed here.
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Reverse cholesterol transport (RCT) has been characterized as a crucial step for antiatherosclerosis, which is initiated by ATP-binding cassette A1 (ABCA1) to mediate the efflux of cellular phospholipids and cholesterol to lipid-free apolipoprotein A-I (apoA-I). However, the mechanisms underlying apoA-I/ABCA1 interaction to lead to the lipidation of apoA-I are poorly understood. There are several models proposed for the interaction of apoA-I with ABCA1 as well as the lipidation of apoA-I mediated by ABCA1. ApoA-I increases the levels of ABCA1 protein markedly. In turn, ABCA1 can stabilize apoA-I. The interaction of apoA-I with ABCA1 could activate signaling molecules that modulate posttranslational ABCA1 activity or lipid transport activity. The key signaling molecules in these processes include protein kinase A (PKA), protein kinase C (PKC), Janus kinase 2 (JAK2), Rho GTPases and Ca²⁺, and many factors also could influence the interaction of apoA-I with ABCA1. This review will summarize these mechanisms for the apoA-I interaction with ABCA1 as well as the signal transduction pathways involved in these processes.
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.