ReviewChronic diseases and translational medicine2015
Tumor necrosis factor-α and its role as a mediator in myocardial infarction: A brief review.
Review in Chronic diseases and translational medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 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
59 citing papers in PubMed, 76 citations in OpenAlex.
- Moderate intensity walking exercises reduce the body mass index and vascular inflammatory factors in postmenopausal women with obesity: a randomized controlled trial.Scientific reports · 2023Trial
- Higher bacterial DNAemia can affect the impact of a polyphenol-rich dietary pattern on biomarkers of intestinal permeability and cardiovascular risk in older subjects.European journal of nutrition · 2022Trial
- TNFR Pathway-Related Proteins and Recurrent Coronary Artery Disease Events.JACC. Advances · 2026Article
- The Mental Health-Acute Coronary Syndrome Continuum: Bidirectional Pathophysiological Links and Clinical Implications.Medical sciences (Basel, Switzerland) · 2026Review
- Targeting cardiac resident CCR2+ macrophage-secreted MCP-1 to attenuate inflammation after myocardial infarction.Acta biomaterialia · 2026Article
- SASP-mediated cellular senescence following myocardial infarction: from spatiotemporal immune regulation to therapeutic strategies.Frontiers in immunology · 2026Review
- Inflammatory Mechanisms in Acute Coronary Syndromes: From Pathophysiology to Therapeutic Targets.Cells · 2025Review
- Systemic Inflammation at the Crossroad of Major Depressive Disorder and Comorbidities: A Narrative Review.International journal of molecular sciences · 2025Review
- MK2 deficiency decreases mortality in male mice during the inflammatory phase after myocardial infarction.Physiological reports · 2025Article
- Pharmacological inhibition of apoptosis, necroptosis, and ferroptosis confers effective cardioprotection in post-myocardial infarction in rats.Scientific reports · 2025Article
- The Role of C-Reactive Protein in Acute Myocardial Infarction: Unmasking Diagnostic, Prognostic, and Therapeutic Insights.Journal of clinical medicine · 2025Review
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- Polarized macrophages modulate cardiac structure and contractility under hypoxia in novel immuno-heart on a chip.APL bioengineering · 2025Article
- Anti-inflammatory effects of proprotein convertase subtilisin/kexin 9 inhibitor therapy in the early phase of acute myocardial infarction.Heart and vessels · 2025Article
- Advances in the Regulation of Inflammatory Mediators in Nitric Oxide Synthase: Implications for Disease Modulation and Therapeutic Approaches.International journal of molecular sciences · 2025Review
- Matrisome remodeling in the myocardium of hypertrophic cardiomyopathy; novel targets for molecular diagnostics.Frontiers in cell and developmental biology · 2025Review
- Potential cardioprotective effect of paroxetine against ventricular remodeling in an animal model of myocardial infarction: a comparative study.BMC pharmacology & toxicology · 2024Article
- Nigella sativa oil attenuates inflammation and oxidative stress in experimental myocardial infarction.BMC complementary medicine and therapies · 2024Article
- Management of a Patient with Cardiovascular Disease Should Include Assessment of Primary and Secondary Immunodeficiencies: Part 2-Secondary Immunodeficiencies.Healthcare (Basel, Switzerland) · 2024Review
- Constructing the dynamic transcriptional regulatory networks to identify phenotype-specific transcription regulators.Briefings in bioinformatics · 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
5 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tumor necrosis factor-α (TNF-α) contributes to myocardial infarction (MI) injury. Polymorphism of TNF-α gene promoter region and secretion and release of TNF-α and its transformation by a series of signaling pathways are all changed at different points of pathophysiological process in MI. Researches also investigated TNF-α antagonists and their potential therapeutic role in the setting of MI and heart failure at both molecular and clinical level. This article briefly reviews TNF-α and its mechanism as a mediator in MI.
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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.