ArticleJournal of cardiovascular translational research2022
Macrophage CD36 and TLR4 Cooperation Promotes Foam Cell Formation and VSMC Migration and Proliferation Under Circadian Oscillations.
Article in Journal of cardiovascular translational research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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
7 citing papers in PubMed, 14 citations in OpenAlex.
- Comprehensive bioinformatics analysis and experimental validation reveal the role of circadian rhythm-related genes in the crosstalk between osteoporosis and atherosclerosis.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Article
- Foam cells: tracing the diverse cellular origins and their linked signaling pathways.Journal of translational medicine · 2025Review
- Extracellular vesicles in atherosclerosis cardiovascular disease: emerging roles and mechanisms.Frontiers in cardiovascular medicine · 2025Review
- The role of protein S-acylation in vascular injury associated with metabolic disorders.Frontiers in endocrinology · 2025Review
- The Nf1-Q181X point mutation induces M2 macrophage polarization via the AKT/STAT pathway to promote smooth muscle cell proliferation and migration.Molecular biology reports · 2024Article
- An update on ox-LDL-inducing vascular smooth muscle cell-derived foam cells in atherosclerosis.Frontiers in cell and developmental biology · 2024Review
- Screening for key genes in circadian regulation in advanced atherosclerosis: A bioinformatic analysis.Frontiers in cardiovascular medicine · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Circadian rhythm disorders can accelerate atherosclerosis. This study aimed to determine the role of circadian disordered macrophages in atherosclerotic development. Mice were divided into NC group (normal circadian rhythm), L24 group (constant light), D12L12 group (weekly shift light/dark cycle), and D24 group (constant dark). Atherosclerotic progression was significantly accelerated in L24, D12L12, and D24 groups. Peritoneal macrophages from circadian disruption groups exhibited enhanced cytokine secretion and foam cell formation. Migration and proliferation of vascular smooth muscle cells (VSMCs) were increased under the conditioned medium of circadian disordered macrophages. The blockade of CD36 markedly inhibited foam cell formation. Compared with blocking CD36 or TLR4 alone, the co-inhibition of CD36 and TLR4 in macrophages further reduced cytokine secretion and more effectively inhibited VSMC migration and proliferation. In conclusion, the activation of CD36 and TLR4 in circadian disordered macrophages promotes foam cell formation and cytokine secretion and enhances VSMC migration and proliferation. Circadian rhythm disorders promote lipid uptake and cytokine secretion of macrophages by regulating CD36 and TLR4, and enhance VSMC migration and proliferation through the paracrine effect of macrophages.
Indexed as
Identifiers
What Socratic 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 Socratic graph.