ReviewJournal of cardiovascular translational research2020
Atherosclerosis: Insights into Vascular Pathobiology and Outlook to Novel Treatments.
Review in Journal of cardiovascular translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 69 citations in OpenAlex.
- Effects of photobiomodulation therapy (PBMT) over endothelial function in healthy individuals: a preliminary crossover clinical trial.Lasers in medical science · 2023Trial
- Vascular calcification: pathogenic mechanisms, signaling crosstalk and translational therapeutics.Signal transduction and targeted therapy · 2026Review
- Discoidin domain receptor 1 (DDR1): An emerged novel mechanosensor.Fundamental research · 2026Review
- Targeting the Hippo pathway in pulmonary arterial hypertension: emerging pharmacological strategies.Journal of hypertension · 2026Review
- Smooth muscle cell phenotypic modulation during atherosclerosis.Vascular pharmacology · 2026Review
- Phenotypic Switching of VSMCs in the Development of CVDs: Focus on miRs.International journal of molecular sciences · 2025Review
- The Crosstalk Between Endothelial Cells, Smooth Muscle Cells, and Macrophages in Atherosclerosis.International journal of molecular sciences · 2025Review
- MiR-140-3p Normalizes Vascular Smooth Muscle Cell Behavior by Inhibiting the RhoA/ROCK Signaling Pathway in Lower-extremity Arteriosclerosis Obliterans.Combinatorial chemistry & high throughput screening · 2025Article
- Bioactive Macromolecule-mediated Biogenic FeONPs Attenuate Inflammation in Atherosclerotic Rat by Activating PI3K/Akt/eNOS Pathway.Current pharmaceutical design · 2025Article
- Uncovering the Role of Anmeidan against Atherosclerosis from Integrated Network Pharmacology and Pharmacological Experiments.Combinatorial chemistry & high throughput screening · 2025Article
- Hormonal influence: unraveling the impact of sex hormones on vascular smooth muscle cells.Biological research · 2024Review
- Cell death in atherosclerosis.Cell cycle (Georgetown, Tex.) · 2024Review
- Role of Circular RNAs in Atherosclerosis through Regulation of Inflammation, Cell Proliferation, Migration, and Apoptosis: Focus on Atherosclerotic Cerebrovascular Disease.Medicina (Kaunas, Lithuania) · 2023Review
- Tan IIA mitigates vascular smooth muscle cell proliferation and migration induced by ox-LDL through the miR-137/TRPC3 axis.The Kaohsiung journal of medical sciences · 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
- Calciphylaxis and its co-occurrence with connective tissue diseases.International wound journal · 2023Review
- Smooth Muscle Cell Phenotypic Switch Induced by Traditional Cigarette Smoke Condensate: A Holistic Overview.International journal of molecular sciences · 2023Article
- Whole genome methylation combined with RNA-seq reveals the protective effects of Gualou-Xiebai herb pair in foam cells through DNA methylation mediated PI3K-AKT signaling pathway.Frontiers in immunology · 2023Article
- Macrophages regulate vascular smooth muscle cell function during atherosclerosis progression through IL-1β/STAT3 signaling.Communications biology · 2022Article
- [Research progress on the regulation of macrophage polarization by mechanical stimulation in wound healing].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 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
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathobiology of atherosclerosis and its current and potential future treatments are summarized, with a spotlight on three central cell types involved: (i) endothelial cells (ECs), (ii) macrophages, and (iii) vascular smooth muscle cells (VSMCs). (i) EC behaviour is regulated by the central transcription factors YAP/TAZ in reaction to biomechanical forces, such as hemodynamic shear stress. (ii) VSMC transdifferentiation (phenotype switching) to a macrophage-like phenotype contributes to the majority of cells positive for common cell surface macrophage markers in atherosclerotic plaques. (iii) Intra-plaque macrophages originate in a significant number from vascular resident macrophages. They can be activated via pattern recognition receptors on cell membrane (e.g. toll-like receptors) and inside cells (e.g. inflammasomes), requiring priming by neutrophil extracellular traps (NETs). ECs and macrophages can also be characterized by single-cell RNA sequencing. Adaptive immunity plays an important role in the inflammatory process. Future therapeutic options include vaccination, TRAF-STOPs, senolysis, or CD47 blockade. Graphical Abstract.
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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.