ArticleStem cell research2021
Functional and molecular effects of TNF-α on human iPSC-derived cardiomyocytes.
Article in Stem cell research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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Who cites it
28 citing papers in PubMed, 32 citations in OpenAlex.
- Deletion of the mouse myocardial Nppb gene alleviates sepsis-induced myocardial dysfunction.Journal of molecular histology · 2026Article
- PD-1/PD-L1 Signaling in Non-ICI Myocarditis.JACC. Basic to translational science · 2026Article
- Refined Carbohydrate-Rich Diet Promotes Early Myocardial Dysfunction Associated with Adiponectin Reduction, Inflammation, and Impaired CaNutrients · 2026Article
- Inflammation-Mediated Mechanisms of Arrhythmias After Acute Myocardial Infarction.Reviews in cardiovascular medicine · 2026Review
- Research progress on coronary heart disease and cytokines: mechanisms, clinical implications, and future directions.Journal of cardiothoracic surgery · 2026Review
- Microfluidic Modeling of Macrophage-Induced Cardiac Inflammation Using NF-κB Reporter Cardiomyocytes.Advanced healthcare materials · 2026Article
- Circulating Biomarkers in Elderly Patients with Heart Failure: A Real-Life Study.Antioxidants (Basel, Switzerland) · 2026Article
- IL-32 as a potential biomarker and therapeutic target in cardiovascular disease.Frontiers in immunology · 2026Review
- Psoriasis and atrial fibrillation: Exploring the intersection.World journal of experimental medicine · 2025Review
- The role of iPSC research for insight into inherited arrhythmia conditions.Heart rhythm · 2025Review
- SGLT2 Inhibitor Might Prevent Atrial Fibrillation Related to Metabolic Syndrome via TNF-α Signaling Pathway: A Bioinformatic Study.Journal of arrhythmia · 2025Article
- Epicardial Adipose Tissue-A Novel Therapeutic Target in Obesity Cardiomyopathy.International journal of molecular sciences · 2025Review
- SERCA2a dysfunction in the pathophysiology of heart failure with preserved ejection fraction: a direct role is yet to be established.Heart failure reviews · 2025Review
- Direct effects of prolonged TNF-α and IL-6 exposure on neural activity in human iPSC-derived neuron-astrocyte co-cultures.Frontiers in cellular neuroscience · 2025Article
- Hypoxia and TNF-alpha modulate extracellular vesicle release from human induced pluripotent stem cell-derived cardiomyocytes.Journal of extracellular vesicles · 2024Article
- Pathophysiological Mechanisms of Psychosis-Induced Atrial Fibrillation: The Links between Mental Disorder and Arrhythmia.Reviews in cardiovascular medicine · 2024Review
- Article
- Equine induced pluripotent stem cells are responsive to inflammatory cytokines before and after differentiation into musculoskeletal cell types.In vitro cellular & developmental biology. Animal · 2023Article
- TNF-α Preconditioning Promotes a Proangiogenic Phenotype in hiPSC-Derived Vascular Smooth Muscle Cells.Cellular and molecular bioengineering · 2023Article
- Fir(e)ing the Rhythm: Inflammatory Cytokines and Cardiac Arrhythmias.JACC. Basic to translational science · 2023Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Proinflammatory molecule tumor necrosis factor alpha (TNF-α) is predominantly elevated in cytokine storm as well as worsening cardiac function. Here we model the molecular and functional effects of TNF-α in cardiomyocytes (CMs) derived from human induced pluripotent stem cells (hiPSC). We found that treatment of hiPSC-CMs with TNF-α increased reactive oxygen species (ROS) and caspase 3/7 activity and caused cell death and apoptosis. TNF-α treatment also resulted in dysregulation of cardiomyocyte function with respect to the increased abnormal calcium handling, calcium wave propagation between cells and excitation-contraction coupling. We also uncovered significant changes in gene expression and protein localization caused by TNF-α treatment. Notably, TNF-α treatment altered the expression of ion channels, dysregulated cadherins, and affected the localization of gap-junction protein connexin-43. In addition, TNF-α treatment up-regulated IL-32 (a human specific cytokine, not present in rodents and an inducer of TNF-α) and IL-34 and down-regulated glutamate receptors and cardiomyocyte contractile proteins. These findings provide insights into the molecular and functional consequences from the exposure of human cardiomyocytes to TNF-α. Our study provides a model to incorporate inflammatory factors into hiPSC-CM-based studies to evaluate mechanistic aspects of heart disease.
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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.