ReviewJournal of the American Heart Association2022
Antiatherosclerotic Effects of CSL112 Mediated by Enhanced Cholesterol Efflux Capacity.
Review in Journal of the American Heart Association, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 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
21 citing papers in PubMed, 30 citations in OpenAlex.
- Apolipoprotein(a)-rich electronegative HDL accelerates vascular aging and atherosclerosis by inducing endothelial senescence.GeroScience · 2026Article
- Inventive HDL Mimicking Nanoparticles: A Promising Frontier in Cardiovascular Disease Management.Cardiovascular toxicology · 2025Review
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Reprogramming Atherosclerosis: Precision Drug Delivery, Nanomedicine, and Immune-Targeted Therapies for Cardiovascular Risk Reduction.Pharmaceutics · 2025Review
- Targeted drug delivery systems for atherosclerosis.Journal of nanobiotechnology · 2025Review
- Reduced high-density lipoprotein antioxidant function in patients with coronary artery disease and acute coronary syndrome.JCI insight · 2025Article
- Quo Vadis after AEGIS: New Opportunities for Therapies Targeted at Reverse Cholesterol Transport?Current atherosclerosis reports · 2025Review
- Adiponectin and Adiponectin Receptors in Atherosclerosis.Endocrine reviews · 2025Review
- Reversal of Atherosclerotic Plaque Growth and Vulnerability: Effects of Lipid-Modifying and Anti-Inflammatory Therapeutic Agents.Biomedicines · 2024Review
- Article
- Ferroptosis and Lipid Metabolism in Acute Myocardial Infarction.Reviews in cardiovascular medicine · 2024Review
- Flipped C-Terminal Ends of APOA1 Promote ABCA1-Dependent Cholesterol Efflux by Small HDLs.Circulation · 2024Article
- Antioxidant and Anti-Inflammatory Functions of High-Density Lipoprotein in Type 1 and Type 2 Diabetes.Antioxidants (Basel, Switzerland) · 2023Review
- Flipped C-Terminal Ends of APOA1 Promote ABCA1-dependent Cholesterol Efflux by Small HDLs.medRxiv : the preprint server for health sciences · 2023Article
- Proteomic Determinants of Variation in Cholesterol Efflux: Observations from the Dallas Heart Study.International journal of molecular sciences · 2023Article
- Novel and future lipid-modulating therapies for the prevention of cardiovascular disease.Nature reviews. Cardiology · 2023Review
- Are we ready for cell-specific therapies in atherosclerosis?European heart journal · 2023Article
- The Impact of MiR-33a-5p Inhibition in Pro-Inflammatory Endothelial Cells.Diseases (Basel, Switzerland) · 2023Article
- Can "Bad" HDL Be Turned Good Again?Arteriosclerosis, thrombosis, and vascular biology · 2023Article
- Emerging Therapies for the Treatment of Atherosclerotic Cardiovascular Disease: From Bench to Bedside.International journal of molecular sciences · 2023Review
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Approximately 12% of patients with acute myocardial infarction (AMI) experience a recurrent major adverse cardiovascular event within 1 year of their primary event, with most occurring within the first 90 days. Thus, there is a need for new therapeutic approaches that address this 90-day post-AMI high-risk period. The formation and eventual rupture of atherosclerotic plaque that leads to AMI is elicited by the accumulation of cholesterol within the arterial intima. Cholesterol efflux, a mechanism by which cholesterol is removed from plaque, is predominantly mediated by apolipoprotein A-I, which is rapidly lipidated to form high-density lipoprotein in the circulation and has atheroprotective properties. In this review, we outline how cholesterol efflux dysfunction leads to atherosclerosis and vulnerable plaque formation, including inflammatory cell recruitment, foam cell formation, the development of a lipid/necrotic core, and degradation of the fibrous cap. CSL112, a human plasma-derived apolipoprotein A-I, is in phase 3 of clinical development and aims to reduce the risk of recurrent cardiovascular events in patients with AMI in the first 90 days after the index event by increasing cholesterol efflux. We summarize evidence from preclinical and clinical studies suggesting that restoration of cholesterol efflux by CSL112 can stabilize plaque by several anti-inflammatory/immune-regulatory processes. These effects occur rapidly and could stabilize vulnerable plaques in patients who have recently experienced an AMI, thereby reducing the risk of recurrent major adverse cardiovascular events in the high-risk early post-AMI period.
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.