ReviewInternational journal of molecular sciences2023
Pathophysiological Effects of Various Interleukins on Primary Cell Types in Common Heart Disease.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 16 citations in OpenAlex.
- Exercise intensity-dependent cardiac telocyte expansion is associated with physiological growth despite JAK/STAT pathway inactivity in male Wistar rats.Experimental physiology · 2026Article
- Curcumol alleviates cardiac and cerebral injury caused by encephalomyocarditis virus (EMCV) in Kunming mice via suppressing NF-κB/NLRP3 inflammasome pathway.Frontiers in pharmacology · 2026Article
- Nuclear factor erythroid 2 related factor 2, tumor necrosis factor alpha, interleukin-40, and endorepellin levels in patients undergoing coronary artery bypass grafting.Revista da Associacao Medica Brasileira (1992) · 2026Article
- Therapeutic Targets for Myocardial Fibrosis: A Comprehensive Review of Current and Emerging Approaches.Cardiovascular & hematological disorders drug targets · 2026Review
- siRNA-mediated inhibition of NTT-MMP-2 reduces oxidative stress and apoptotic signaling in an ex vivo model of ischemia/reperfusion injury.Scientific reports · 2025Article
- Role of HMGB1 in ischemia/reperfusion injury in a rat model of myocardial infarction.Scientific reports · 2025Article
- Inflammasomes as Potential Therapeutic Targets to Prevent Chronic Active Viral Myocarditis-Translating Basic Science into Clinical Practice.International journal of molecular sciences · 2025Review
- MiR-1291 mediates the protective effect of sevoflurane preconditioning against hypoxia/reoxygenation-induced myocardial cell injury.Toxicology research · 2025Article
- Current anti-inflammatory strategies for treatment of heart failure: From innate to adaptive immunity.Pharmacological research · 2025Review
- The Potential Contribution of the IL-37/IL-18/IL-18BP/IL-18R Axis in the Pathogenesis of Sjögren's Syndrome.International journal of molecular sciences · 2025Article
- Cytokine Adsorption During Ex Vivo Blood Perfusion Improves Contractility of Donation After Circulatory Death Hearts.Journal of the American Heart Association · 2024Article
- The impact of inflammatory and oxidative stress biomarkers on the sympathetic nervous system in severe coronary atherosclerosis.Frontiers in cardiovascular medicine · 2024Article
- Protective effect of canagliflozin on post-resuscitation myocardial function in a rat model of cardiac arrest.Intensive care medicine experimental · 2023Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Myocardial infarction (MI), heart failure, cardiomyopathy, myocarditis, and myocardial ischemia-reperfusion injury (I/R) are the most common heart diseases, yet there is currently no effective therapy due to their complex pathogenesis. Cardiomyocytes (CMs), fibroblasts (FBs), endothelial cells (ECs), and immune cells are the primary cell types involved in heart disorders, and, thus, targeting a specific cell type for the treatment of heart disease may be more effective. The same interleukin may have various effects on different kinds of cell types in heart disease, yet the exact role of interleukins and their pathophysiological pathways on primary cell types remain largely unexplored. This review will focus on the pathophysiological effects of various interleukins including the IL-1 family (IL-1, IL-18, IL-33, IL-37), IL-2, IL-4, the IL-6 family (IL-6 and IL-11), IL-8, IL-10, IL-17 on primary cell types in common heart disease, which may contribute to the more precise and effective treatment of heart disease.
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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.