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.
Highlights
Cadmium is an environmental pollutant and a highly toxic metal ion, accumulated largely in the liver and kidney [1,2]
Since cardiomyocytes were highly dependent on energy productions, cadmium toxicity disrupted glucose consumptions and utilizations through inhibiting AKT/mammalian target of rapamycin (mTOR) pathway
Considering that glucose oxidation primarily occurs in mitochondria, we would like to confirm whether mitochondria respiratory gene expression is altered by cadmium toxicity in cardiomyocytes
Summary
Cadmium is an environmental pollutant and a highly toxic metal ion, accumulated largely in the liver and kidney [1,2]. Studies in animals or cultured cells have implicated cadmium in aetiology and pathogenesis of hypertension and toxicity [8,9,10]. To meet the energy demand in the heart, energy production of the heart is primarily dependent on mitochondria for ATP production by glucose oxidation [12]. Many metabolites involved in cardiac energy metabolism are held constant in homoeostasis over the range of normal physiological condition, environmental toxicity and cell stress may imbalance the metabolic homoeostasis and disrupt the energy production in the heart. Once the energy production is blocked (e.g., by ischaemia or hypoxia), metabolic homoeostasis of the heart may be impaired, leading to cardiac cell death and various cardiovascular diseases [13]
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