ReviewMolecular and cellular biochemistry2023
Role of oncostatin-M in ECM remodeling and plaque vulnerability.
Review in Molecular and cellular biochemistry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 21 citations in OpenAlex.
- Critical Assessment of Optimal Timing to Initiate Post-Stroke Rehabilitation.Archives of internal medicine research · 2026Article
- Reducing CETP activity prevents memory decline in an Alzheimer's disease mouse model.EMBO molecular medicine · 2026Article
- Tear Cytokine Signature in Vernal Keratoconjunctivitis: A Chemokine-Remodeling Axis Associated with Disease Severity.International journal of molecular sciences · 2026Article
- Circulating cfdna: A novel biomarker for preventing early recurrence in ischemic stroke.Journal of thrombosis and thrombolysis · 2026Review
- Uncovering Potential Druggable Targets in Coronary Atherosclerosis: A Proteome-Wide Mendelian Randomization Study With Cross-Platform and Experimental Validation.Cardiovascular therapeutics · 2026Article
- Integrative blood profiling uncovers inflammatory network signatures in high-altitude pulmonary edema.Bioscience reports · 2025Article
- The Dual Role of ADAMTS1 in Cardiovascular Remodeling: Balancing Extracellular Matrix Homeostasis and Pathological States.Journal of cardiovascular development and disease · 2025Review
- Myocardial transcriptomic and proteomic landscapes across the menopausal continuum in a murine model of chemically induced accelerated ovarian failure.Physiological genomics · 2025Article
- The IL-22-oncostatin M axis promotes intestinal inflammation and tumorigenesis.Nature immunology · 2025Article
- Apolipoprotein B in the Risk Assessment, Diagnosis, and Treatment of Cardiometabolic Diseases.Cardiology and cardiovascular medicine · 2025Article
- ECM-dependent regulation of septin 7 in focal adhesions promotes mechanosensing and functional response in fibroblasts.iScience · 2024Article
- Novel Factors Regulating Proliferation, Migration, and Differentiation of Fibroblasts, Keratinocytes, and Vascular Smooth Muscle Cells during Wound Healing.Biomedicines · 2024Review
- Epidemiology, Pathophysiology, and Current Treatment Strategies in Stroke.Cardiology and cardiovascular medicine · 2024Article
- Targeting Oncostatin M Receptor to Attenuate Carotid Artery Plaque Vulnerability in Hypercholesterolemic Microswine.Cardiology and cardiovascular medicine · 2024Article
- Therapeutic Potential of Targeting p27Archives of internal medicine research · 2024Article
- PCSK9i promoting the transformation of AS plaques into a stable plaque by targeting the miR-186-5p/Wipf2 and miR-375-3p/Pdk1/Yap1 in ApoE-/- mice.Frontiers in medicine · 2024Article
- Residual risks and evolving atherosclerotic plaques.Molecular and cellular biochemistry · 2023Review
- Tear Fluid Inflammatory Proteome Analysis Highlights Similarities Between Keratoconus and Allergic Conjunctivitis.Investigative ophthalmology & visual science · 2023Article
- Pro-Inflammatory Biomarkers and Progression of Atherosclerosis in Patients with Myocardial Infarction with Non-Obstructive Coronary Artery Disease: 1-Year Follow-Up.Journal of personalized medicine · 2023Article
- In Search of the Perfect Marker.Arquivos brasileiros de cardiologia · 2023Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Atherosclerosis is a multifactorial inflammatory disease characterized by the development of plaque formation leading to occlusion of the vessel and hypoxia of the tissue supplied by the vessel. Chronic inflammation and altered collagen expression render stable plaque to unstable and increase plaque vulnerability. Thinned and weakened fibrous cap results in plaque rupture and formation of thrombosis and emboli formation leading to acute ischemic events such as stroke and myocardial infarction. Inflammatory mediators including TREM-1, TLRs, MMPs, and immune cells play a critical role in plaque vulnerability. Among the other inflammatory mediators, oncostatin-M (OSM), a pro-inflammatory cytokine, play an important role in the development and progression of atherosclerosis, however, the role of OSM in plaque vulnerability and extracellular matrix remodeling (ECM) is not well understood and studied. Since ECM remodeling plays an important role in atherosclerosis and plaque vulnerability, a detailed investigation on the role of OSM in ECM remodeling and plaque vulnerability is critical. This is important because the role of OSM has been discussed in the context of proliferation of vascular smooth muscle cells and regulation of cytokine expression but the role of OSM is scarcely discussed in relation to ECM remodeling and plaque vulnerability. This review focuses on critically discussing the role of OSM in ECM remodeling and plaque vulnerability.
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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.