ReviewArteriosclerosis, thrombosis, and vascular biology2024
Prostanoids in Cardiac and Vascular Remodeling.
Review in Arteriosclerosis, thrombosis, and vascular biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 19 citations in OpenAlex.
- Endogenous Lipid Signals in Energy Homeostasis and Fibrosis.Biomolecules · 2026Review
- Atrial Fibrillation in a Young Patient Using High-dose Oral Diclofenac: A Case Report.Clinical practice and cases in emergency medicine · 2026Article
- EIF2α-ATF4-CHAC1 Signalling Links ER Stress to Ferroptosis in Human Aortic Smooth Muscle Cells: Mechanistic Insights and Therapeutic Implications.Journal of cellular and molecular medicine · 2026Article
- Catalytic and structural comparisons of linoleate dioxygenases and their cytochrome P450 companions with enzymes of the cyclooxygenase cascade.The Journal of biological chemistry · 2026Review
- Disruption of sphingolipid metabolism triggers lung vascular inflammation and aging-like changes under hypoxia through VDAC1-mediated mitochondrial DNA release.Apoptosis : an international journal on programmed cell death · 2026Article
- Acupotomy for Cervical Spondylosis-Related Neck Pain: A Study Protocol for a Randomized Controlled Trial.Journal of pain research · 2026Article
- The dual pathological roles and targeted therapy of PGEFrontiers in pharmacology · 2026Review
- Prostaglandins and the Cardiovascular System.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- Hypopituitarism Induced by Continuous Infusion of PGI2 Analogues: A Case Series and the Role of ACTH Screening and Hydrocortisone Treatment.Pulmonary circulation · 2025Article
- Targeting the E Prostanoid Receptor EP4 Mitigates Cardiac Fibrosis Induced by β-Adrenergic Activation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- CD44 as a novel therapeutic target in pulmonary arterial hypertension: Insights from multi-omics integration and molecular docking.PloS one · 2025Article
- Epidemiology, risk factors and mechanism of breast cancer and atrial fibrillation.Cardio-oncology (London, England) · 2024Review
- PAC1 Agonist Maxadilan Reduces Atherosclerotic Lesions in Hypercholesterolemic ApoE-Deficient Mice.International journal of molecular sciences · 2024Article
- Molecular Thumbprints: Biological Signatures That Measure Loss of Identity.Biomolecules · 2024Article
- Pain from Internal Organs and Headache: The Challenge of Comorbidity.Diagnostics (Basel, Switzerland) · 2024Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Prostanoids are biologically active lipids generated from arachidonic acid by the action of the COX (cyclooxygenase) isozymes. NSAIDs, which reduce the biosynthesis of prostanoids by inhibiting COX activity, are effective anti-inflammatory, antipyretic, and analgesic drugs. However, their use is limited by cardiovascular adverse effects, including myocardial infarction, stroke, hypertension, and heart failure. While it is well established that NSAIDs increase the risk of atherothrombotic events and hypertension by suppressing vasoprotective prostanoids, less is known about the link between NSAIDs and heart failure risk. Current evidence indicates that NSAIDs may increase the risk for heart failure by promoting adverse myocardial and vascular remodeling. Indeed, prostanoids play an important role in modulating structural and functional changes occurring in the myocardium and in the vasculature in response to physiological and pathological stimuli. This review will summarize current knowledge of the role of the different prostanoids in myocardial and vascular remodeling and explore how maladaptive remodeling can be counteracted by targeting specific prostanoids.
Indexed as
Identifiers
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.