ReviewCurrent atherosclerosis reports2004
Matrix metalloproteinases and atherosclerosis.
Review in Current atherosclerosis reports, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
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
49 citing papers in PubMed, 1 synthesis or guideline pooled it, 131 citations in OpenAlex.
- Modeling vascular inflammation and atherogenicity after inhalation of ambient levels of ozone: exploratory lessons from transcriptomics.Inhalation toxicology · 2017Pooled it
- Nicorandil suppresses the increases in plasma level of matrix metalloproteinase activity and attenuates left ventricular remodeling in patients with acute myocardial infarction.Heart and vessels · 2007Trial
- Pharmacological considerations for next-generation protein therapeutics in cardiovascular disease.The Journal of pharmacology and experimental therapeutics · 2025Review
- Reconceptualizing Endothelial-to-mesenchymal transition in atherosclerosis: Signaling pathways and prospective targeting strategies.Journal of advanced research · 2025Review
- Paroxetine suppresses 27-hydroxycholesterol-induced responses in THP-1 human monocytic cells by regulating the AKT/mTORC1 pathway.Scientific reports · 2025Article
- Epithelial sodium channel in dendritic cells participates in high-fat-induced inflammatory responses.Molecular biology reports · 2025Article
- Role of annexin A7 in the occurrence and progression of coronary atherosclerosis: a narrative review.Cardiovascular diagnosis and therapy · 2025Review
- Polymeric Nanomaterials for Atherosclerosis Diagnosis and Treatment.Polymer science & technology (Washington, D.C.) · 2025Review
- Incretin-based therapies for the management of cardiometabolic disease in the clinic: Past, present, and future.Medicinal research reviews · 2025Review
- Hydrogen Sulfide Modulation of Matrix Metalloproteinases and CD147/EMMPRIN: Mechanistic Pathways and Impact on Atherosclerosis Progression.Biomedicines · 2024Review
- Roles of lncRNAs in NF-κB-Mediated Macrophage Inflammation and Their Implications in the Pathogenesis of Human Diseases.International journal of molecular sciences · 2024Review
- Proteomics Studies Suggest That Nitric Oxide Donor Furoxans Inhibit In Vitro Vascular Smooth Muscle Cell Proliferation by Nitric Oxide-Independent Mechanisms.Molecules (Basel, Switzerland) · 2023Article
- Potential Treatment Options for Neuroblastoma with Polyphenols through Anti-Proliferative and Apoptotic Mechanisms.Biomolecules · 2023Review
- The Influence of Dietary Interventions on Arterial Stiffness in Overweight and Obese Subjects.Nutrients · 2023Review
- Mesenchymal stem cells in ischemic tissue regeneration.World journal of stem cells · 2023Review
- Targeting Immune Senescence in Atherosclerosis.International journal of molecular sciences · 2022Review
- Matrix Metalloproteinase-9 as an Important Contributor to the Pathophysiology of Depression.Frontiers in neurology · 2022Review
- Article
- Stem Cell Based Approaches to Modulate the Matrix Milieu in Vascular Disorders.Frontiers in cardiovascular medicine · 2022Review
- Time-resolved Fluorescence Immunoassay (TRFIA) for the Simultaneous Detection of MMP-9 and Lp-PLA2 in Serum.Journal of fluorescence · 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
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis is a major cause of coronary heart disease, and matrix metalloproteinases (MMPs) play an important role in atherosclerosis by degrading the extracellular matrix, which results in cardiovascular remodeling. Recent studies have identified enhanced expression of MMPs in the atherosclerotic lesion and their contribution to weakening of the vascular wall by degrading the extracellular matrix. The transcription, enzyme processing, and specific inhibition of MMPs by tissue inhibitors of matrix metalloproteinase (TIMPs) regulate these effects. These processes are also modified by inflammatory cytokines and cell-cell contact signaling. Both animal experiments and clinical sample analysis have shown that balance in expression and activation of MMPs and inhibition by TIMPs is critical for the development of stenotic and aneurysmal change. Polymorphism in the MMP gene promoter contributes to inter-individual differences in susceptibility to coronary heart disease. The development of therapeutic drugs specifically targeting MMPs may thus be useful for the prevention of atherosclerotic lesion progression, plaque rupture, and restenosis.
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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.