ArticleBasic research in cardiology2020
Inhibition of macrophage proliferation dominates plaque regression in response to cholesterol lowering.
Article in Basic research in cardiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 76 citations in OpenAlex.
- Aggressive cholesterol lowering normalizes atherosclerosis regression in Jak2Journal of lipid research · 2026Article
- Non-high-density lipoprotein cholesterol to high-density lipoprotein cholesterol ratio in relation to erectile dysfunction: a cross-sectional study.Translational andrology and urology · 2026Article
- NLRP3 mediates lipid-driven macrophage proliferation in established atherosclerosis.Basic research in cardiology · 2025Article
- GATA2 Mediates Macrophage Proliferation During Atherosclerosis.Journal of the American Heart Association · 2025Article
- Mitigating atherosclerosis: Integrating vaccines with gene targets.American heart journal plus : cardiology research and practice · 2025Review
- Article
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- Nonpreferential but Detrimental Accumulation of Macrophages With Clonal Hematopoiesis-Driver Mutations in Cardiovascular Tissues-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- In Vitro Targeted Delivery of Simvastatin and Niacin to Macrophages Using Mannan-Grafted Magnetite Nanoparticles.ACS omega · 2024Article
- The role of M1/M2 macrophage polarization in the pathogenesis of obesity-related kidney disease and related pathologies.Frontiers in immunology · 2024Review
- Immune Homeostasis Maintenance Through Advanced Immune Therapeutics to Target Atherosclerosis.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Clonal Expansion in Cardiovascular Pathology.JACC. Basic to translational science · 2024Review
- X chromosome inactivation skewing is common in advanced carotid atherosclerotic lesions in females and predicts secondary peripheral artery events.Biology of sex differences · 2023Article
- The Impact of Exercise on Immunity, Metabolism, and Atherosclerosis.International journal of molecular sciences · 2023Review
- Emerging Concepts of Vascular Cell Clonal Expansion in Atherosclerosis.Arteriosclerosis, thrombosis, and vascular biology · 2022Review
- YB1 dephosphorylation attenuates atherosclerosis by promoting CCL2 mRNA decay.Frontiers in cardiovascular medicine · 2022Article
- Macrophages in Atheromatous Plaque Developmental Stages.Frontiers in cardiovascular medicine · 2022Review
- ATP5O Hypo-crotonylation Caused by HDAC2 Hyper-Phosphorylation Is a Primary Detrimental Factor for Downregulated Phospholipid Metabolism under Chronic Stress.Research (Washington, D.C.) · 2022Article
- Everolimus-Loaded Reconstituted High-Density Lipoprotein Prepared by a Novel Dual Centrifugation Approach for Anti-Atherosclerotic Therapy.International journal of nanomedicine · 2022Article
- Impact of Acute and Chronic Psychosocial Stress on Vascular Inflammation.Antioxidants & redox signaling · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
29 authors at 6 institutions in 6 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Statins induce plaque regression characterized by reduced macrophage content in humans, but the underlying mechanisms remain speculative. Studying the translational APOE*3-Leiden.CETP mouse model with a humanized lipoprotein metabolism, we find that systemic cholesterol lowering by oral atorvastatin or dietary restriction inhibits monocyte infiltration, and reverses macrophage accumulation in atherosclerotic plaques. Contrary to current believes, none of (1) reduced monocyte influx (studied by cell fate mapping in thorax-shielded irradiation bone marrow chimeras), (2) enhanced macrophage egress (studied by fluorescent bead labeling and transfer), or (3) atorvastatin accumulation in murine or human plaque (assessed by mass spectrometry) could adequately account for the observed loss in macrophage content in plaques that undergo phenotypic regression. Instead, suppression of local proliferation of macrophages dominates phenotypic plaque regression in response to cholesterol lowering: the lower the levels of serum LDL-cholesterol and lipid contents in murine aortic and human carotid artery plaques, the lower the rates of in situ macrophage proliferation. Our study identifies macrophage proliferation as the predominant turnover determinant and an attractive target for inducing plaque regression.
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.