ReviewFrontiers in cell and developmental biology2022
Matrix Vesicles as a Therapeutic Target for Vascular Calcification.
Review in Frontiers in cell and developmental biology, 2022. 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, 36 citations in OpenAlex.
- Coronary Calcified Nodules: From Pathological Definitions to Intravascular Imaging- and Morphology-Guided PCI.International journal of molecular sciences · 2026Review
- Coronary Artery Calcification: From Molecular Mechanisms to Interventional Strategies.International journal of molecular sciences · 2026Review
- Gla-Rich Protein Across the Chronic Kidney Disease Spectrum: Association with Vascular Calcification Burden and CKD-MBD Disturbances.Journal of clinical medicine · 2026Article
- Distinct types of regulated cell death in atherosclerosis.Journal of pharmaceutical analysis · 2026Review
- Aging-Driven Inter-Organ Crosstalk in Postmenopausal Osteoporosis: From Immunometabolic Drift to Multisystem Frailty.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Review
- Osteoporosis therapies and coronary risk: insights from vascular calcification biology and sclerostin signaling.Frontiers in endocrinology · 2026Review
- Uric acid-associated mechanisms of coronary artery calcification in diabetic kidney disease: evidence, hypotheses, and translational perspectives.Frontiers in cardiovascular medicine · 2026Review
- Biomechanics of Plaque Rupture and Cardiovascular Calcification.Advances in experimental medicine and biology · 2026Review
- Vascular Calcification in Chronic Kidney Disease and Hemodialysis: Pathophysiological Mechanisms and Emerging Biomarkers.Medicina (Kaunas, Lithuania) · 2025Review
- Exosomal non-coding RNAs: key regulators of inflammation-related cardiovascular disorders.European journal of medical research · 2025Review
- Building a digital library on research into mineralizing vesicles: a systematic review-based approach.Biophysical reviews · 2025Review
- Endothelial cells under disturbed flow release extracellular vesicles to promote inflammatory polarization of macrophages and accelerate atherosclerosis.BMC biology · 2025Article
- From Cells to Plaques: The Molecular Pathways of Coronary Artery Calcification and Disease.Journal of clinical medicine · 2024Review
- Mechanisms of Cardiovascular Calcification and Experimental Models: Impact of Vitamin K Antagonists.Journal of clinical medicine · 2024Review
- Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities.Biomolecules · 2024Review
- The role and applications of extracellular vesicles in osteoporosis.Bone research · 2024Review
- Review
- Interstitial Fluid Shear Stress Induces the Synthetic Phenotype Switching of VSMCs to Release Pro-calcified Extracellular Vesicles via EGFR-MAPK-KLF5 Pathway.International journal of biological sciences · 2024Article
- Quantitative Assessment of Intracellular Effectors and Cellular Response in RAGE Activation.Archives of internal medicine research · 2024Article
- Associations between pan-immune-inflammation value and abdominal aortic calcification: a cross-sectional study.Frontiers in immunology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Vascular calcification (VC) is linked to an increased risk of heart disease, stroke, and atherosclerotic plaque rupture. It is a cell-active process regulated by vascular cells rather than pure passive calcium (Ca) deposition. In recent years, extracellular vesicles (EVs) have attracted extensive attention because of their essential role in the process of VC. Matrix vesicles (MVs), one type of EVs, are especially critical in extracellular matrix mineralization and the early stages of the development of VC. Vascular smooth muscle cells (VSMCs) have the potential to undergo phenotypic transformation and to serve as a nucleation site for hydroxyapatite crystals upon extracellular stimulation. However, it is not clear what underlying mechanism that MVs drive the VSMCs phenotype switching and to result in calcification. This article aims to review the detailed role of MVs in the progression of VC and compare the difference with other major drivers of calcification, including aging, uremia, mechanical stress, oxidative stress, and inflammation. We will also bring attention to the novel findings in the isolation and characterization of MVs, and the therapeutic application of MVs in VC.
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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.