ReviewCells2020
Signaling Pathways and Key Genes Involved in Regulation of foam Cell Formation in Atherosclerosis.
Review in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 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
45 citing papers in PubMed, 101 citations in OpenAlex.
- Stacked human aortic endothelial cells induce atherosclerotic fatty streaks and release proinflammatory cytokines and chemokines.Mechanobiology in medicine · 2026Article
- Qinggan Jianpi formula attenuates atherosclerosis by suppressing macrophage lactate transport to activate repair genes via H3K18 lactylation.Chinese medicine · 2026Article
- GFPT2 promotes macrophage dysfunction in atherosclerosis via ACADL glycosylation-dependent suppression of ACADL and Arg1.Cellular and molecular life sciences : CMLS · 2026Article
- Emerging insights into inflammation-driven atherosclerosis: immune cell mechanisms.Frontiers in cardiovascular medicine · 2026Review
- Microbiota-innate immune crosstalk drives atherosclerosis: mechanisms, disease progression, and emerging therapeutic strategies.Frontiers in immunology · 2026Review
- Chronic hyperglycemia and cardiovascular dysfunction: an in-depth exploration of metabolic and cellular pathways in type 2 diabetes mellitus.Cardiovascular diabetology. Endocrinology reports · 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
- Atherosclerosis: from lipid-lowering and anti-inflammatory therapies to targeting arterial retention of ApoB-containing lipoproteins.Frontiers in immunology · 2025Review
- The interplay between diabetes and atherosclerosis: A review of pathophysiological mechanisms.ARYA atherosclerosis · 2025Review
- Exosomal non-coding RNAs: key molecules in the diagnosis and treatment of coronary artery disease.PeerJ · 2025Review
- Modification macrophage to foam cells in atherosclerosis disease: some factors stimulate or inhibit this process.Journal of diabetes and metabolic disorders · 2024Review
- Research progress on the therapeutic effects of nanoparticles loaded with drugs against atherosclerosis.Cardiovascular drugs and therapy · 2024Review
- Nobiletin alleviates atherosclerosis by inhibiting lipid uptake via the PPARG/CD36 pathway.Lipids in health and disease · 2024Article
- Increasing Soluble P-Selectin Levels Predict Higher Peripheral Atherosclerotic Plaque Progression.Journal of clinical medicine · 2023Article
- Cellular crosstalk in atherosclerotic plaque microenvironment.Cell communication and signaling : CCS · 2023Review
- CORM-A1 Alleviates Pro-Atherogenic Manifestations via miR-34a-5p Downregulation and an Improved Mitochondrial Function.Antioxidants (Basel, Switzerland) · 2023Article
- Prospects of potential adipokines as therapeutic agents in obesity-linked atherogenic dyslipidemia and insulin resistance.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2023Review
- Macrophage polarization states in atherosclerosis.Frontiers in immunology · 2023Review
- Identification and validation of hub genes involved in foam cell formation and atherosclerosis developmentPeerJ · 2023Article
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 5 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is associated with acute cardiovascular conditions, such as ischemic heart disease, myocardial infarction, and stroke, and is the leading cause of morbidity and mortality worldwide. Our understanding of atherosclerosis and the processes triggering its initiation is constantly improving, and, during the last few decades, many pathological processes related to this disease have been investigated in detail. For example, atherosclerosis has been considered to be a chronic inflammation triggered by the injury of the arterial wall. However, recent works showed that atherogenesis is a more complex process involving not only the immune system, but also resident cells of the vessel wall, genetic factors, altered hemodynamics, and changes in lipid metabolism. In this review, we focus on foam cells that are crucial for atherosclerosis lesion formation. It has been demonstrated that the formation of foam cells is induced by modified low-density lipoprotein (LDL). The beneficial effects of the majority of therapeutic strategies with generalized action, such as the use of anti-inflammatory drugs or antioxidants, were not confirmed by clinical studies. However, the experimental therapies targeting certain stages of atherosclerosis, among which are lipid accumulation, were shown to be more effective. This emphasizes the relevance of future detailed investigation of atherogenesis and the importance of new therapies development.
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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.