ArticleBioscience reports2015
Cadmium toxicity induces ER stress and apoptosis via impairing energy homoeostasis in cardiomyocytes.
Article in Bioscience reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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
29 citing papers in PubMed, 79 citations in OpenAlex.
- Heavy metal toxicity as a driver of endoplasmic reticulum stress and dysfunction.The FEBS journal · 2026Review
- Bio and Geno-toxic Activities of Cadmium- Arsenic Salts Combination And/or Fluoride in Female Rats Confirmed by Molecular Docking.Biological trace element research · 2026Article
- Sublethal cadmium exposure disrupts cardiac function and tissue structure in zebrafish larvae.Frontiers in physiology · 2026Article
- Accumulation and Distribution Characteristics of Cd in the Soil-Plants (Basel, Switzerland) · 2025Article
- Cadmium toxicity on endoplasmic reticulum functioning.International journal of biochemistry and molecular biology · 2024Review
- Review
- Contaminant Metals and Cardiovascular Health.Journal of cardiovascular development and disease · 2023Review
- Monitoring leaching of CdBiosensors & bioelectronics · 2023Article
- Mechanisms of Cd-Induced Cytotoxicity in Normal Human Skin Keratinocytes: Implication for Human Health.International journal of molecular sciences · 2022Article
- Misuse of Cardiac Lipid upon Exposure to Toxic Trace Elements-A Focused Review.Molecules (Basel, Switzerland) · 2022Review
- Cloning and expressions of chop in loach (Misgurnus anguillicaudatus) and its response to hydrogen peroxide (HFish physiology and biochemistry · 2022Article
- Sex differences in the effects of whole-life, low-dose cadmium exposure on postweaning high-fat diet-induced cardiac pathogeneses.The Science of the total environment · 2022Article
- Concurrent Heavy Metal Exposures and Idiopathic Dilated Cardiomyopathy: A Case-Control Study from the Katanga Mining Area of the Democratic Republic of Congo.International journal of environmental research and public health · 2021Article
- Pathophysiological Basis for Nutraceutical Supplementation in Heart Failure: A Comprehensive Review.Nutrients · 2021Review
- Toxic Mechanisms of Five Heavy Metals: Mercury, Lead, Chromium, Cadmium, and Arsenic.Frontiers in pharmacology · 2021Review
- Cadmium sulfate induces apoptosis in planarians.Environmental science and pollution research international · 2020Article
- Protective effect of quercetin on rat testes against cadmium toxicity by alleviating oxidative stress and autophagy.Environmental science and pollution research international · 2020Article
- DomesticatedGenes · 2020Article
- Cadmium-Induced Cytotoxicity: Effects on Mitochondrial Electron Transport Chain.Frontiers in cell and developmental biology · 2020Review
- Changes in rat myocardium contractility under subchronic intoxication with lead and cadmium salts administered alone or in combination.Toxicology reports · 2020Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cadmium, a highly toxic environmental pollutant, is reported to induce toxicity and apoptosis in multiple organs and cells, all possibly contributing to apoptosis in certain pathophysiologic situations. Previous studies have described that cadmium toxicity induces biochemical and physiological changes in the heart and finally leads to cardiac dysfunctions, such as decreasing contractile tension, rate of tension development, heart rate, coronary flow rate and atrioventricular node conductivity. Although many progresses have been made, the mechanism responsible for cadmium-induced cellular alternations and cardiac toxicity is still not fully understood. In the present study, we demonstrated that cadmium toxicity induced dramatic endoplasmic reticulum (ER) stress and impaired energy homoeostasis in cultured cardiomyocytes. Moreover, cadmium toxicity may inhibit protein kinase B (AKT)/mTOR (mammalian target of rapamycin) pathway to reduce energy productions, by either disrupting the glucose metabolism or inhibiting mitochondrial respiratory gene expressions. Our work will help to reveal a novel mechanism to clarify the role of cadmium toxicity to cardiomyocytes and provide new possibilities for the treatment of cardiovascular diseases related to cadmium toxicity.
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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.