ArticleJournal of cellular and molecular medicine2018
Modelling cadmium-induced cardiotoxicity using human pluripotent stem cell-derived cardiomyocytes.
Article in Journal of cellular and molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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.
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Who cites it
26 citing papers in PubMed, 52 citations in OpenAlex.
- Metal Homeostasis Imbalance as Potentially Contributing Mechanism in Onset of Cardiac Disorders in Individuals with Chronic Obstructive Pulmonary Disease and Chronic Kidney Disease.Biological trace element research · 2026Article
- Potentially Toxic Elements-mediated Toxicity on Vagus Nerve and Cellular Energy Expenditure in Noncommunicable Diseases: A Systematic Review and Evidence Map.Biological trace element research · 2026Review
- Molecular Mechanisms of Effects of Lead and Cadmium Co-exposure on Atrial and Ventricular Myocardium: Soluble Salts Versus Nanoparticles.Cardiovascular toxicology · 2026Article
- Dirty Earth, Diseased Hearts: Soil, Water, and Plastic Pollution in the Cardiovascular Exposome.Anatolian journal of cardiology · 2026Article
- Sex-Specific Associations Between Cadmium Exposure and Mortality Risk in Cardiovascular Disease Patients: A Cohort Study Integrating Molecular Mechanisms of Myocardial Dysfunction.Cardiovascular toxicology · 2026Article
- Transcriptomics and metabolomics reveal functional nanoplastics-induced male reproductive damage and resveratrol antagonistic effects.Journal of nanobiotechnology · 2026Article
- ROS-induced degradation of hERG potassium channels contributes to aripiprazole-induced prolongation of the QTc interval.Acta pharmacologica Sinica · 2026Article
- Article
- Cadmium and selenium blood levels in association with congestive heart failure in diabetic and prediabetic patients: a cross-sectional study from the national health and nutrition examination survey.Diabetology & metabolic syndrome · 2025Article
- Beyond glycemic control: the cardiac and hepatic benefits of SGLT2 and DPP-4 inhibitors in mitigating chronic cadmium-induced inflammation, oxidative/nitrative stress, apoptosis and fibrosis.Frontiers in physiology · 2025Article
- Environmental Heavy Metal Exposure and Associated Cardiovascular Diseases in Light of the Triglyceride Glucose Index.Cardiovascular toxicology · 2024Review
- Exposome and unhealthy aging: environmental drivers from air pollution to occupational exposures.GeroScience · 2023Review
- Contaminant Metals as Cardiovascular Risk Factors: A Scientific Statement From the American Heart Association.Journal of the American Heart Association · 2023Article
- Review
- Direct Effects of Toxic Divalent Cations on Contractile Proteins with Implications for the Heart: Unraveling Mechanisms of Dysfunction.International journal of molecular sciences · 2023Review
- Overexpression of KCNJ2 enhances maturation of human-induced pluripotent stem cell-derived cardiomyocytes.Stem cell research & therapy · 2023Article
- Cardiac Development in the Presence of Cadmium: AnEnvironmental health perspectives · 2022Article
- A Novel 3-Gene Signature for Identifying COVID-19 Patients Based on Bioinformatics and Machine Learning.Genes · 2022Article
- A phenome-wide bidirectional Mendelian randomization analysis of atrial fibrillation.International journal of epidemiology · 2022Article
- Cadmium exposure induces cardiac glucometabolic dysregulation and lipid accumulation independent of pyruvate dehydrogenase activity.Annals of medicine · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cadmium, a highly ubiquitous toxic heavy metal, has been widely recognized as an environmental and industrial pollutant, which confers serious threats to human health. The molecular mechanisms of the cadmium-induced cardiotoxicity (CIC) have not been studied in human cardiomyocytes at the cellular level. Here we showed that human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs) can recapitulate the CIC at the cellular level. The cadmium-treated hPSC-CMs exhibited cellular phenotype including reduced cell viability, increased apoptosis, cardiac sarcomeric disorganization, elevated reactive oxygen species, altered action potential profile and cardiac arrhythmias. RNA-sequencing analysis revealed a differential transcriptome profile and activated MAPK signalling pathway in cadmium-treated hPSC-CMs, and suppression of P38 MAPK but not ERK MAPK or JNK MAPK rescued CIC phenotype. We further identified that suppression of PI3K/Akt signalling pathway is sufficient to reverse the CIC phenotype, which may play an important role in CIC. Taken together, our data indicate that hPSC-CMs can serve as a suitable model for the exploration of molecular mechanisms underlying CIC and for the discovery of CIC cardioprotective drugs.
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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.