title: Cadmium toxicity induces ER stress and apoptosis via impairing energy homoeostasis in cardiomyocytes.
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.
authors.affiliation: Department of Geriatrics, The People's Hospital of Zhengzhou, Zhengzhou 450012, China.
authors.forename: Chun-Yan
authors.initials: CY
authors.lastname: Chen
authors.affiliation: Department of Cardiology, the First Affiliated Hospital of Xinxiang Medical University, No. 88, Rd. Jiankang, Xinxiang 453100, China.
authors.forename: Shao-Li
authors.initials: SL
authors.lastname: Zhang
authors.affiliation: Department of internal medicine, The People's Hospital of Dezhou, Dezhou 253014, China.
authors.forename: Zhi-Yong
authors.initials: ZY
authors.lastname: Liu
authors.affiliation: Department of Geriatrics, The People's Hospital of Zhengzhou, Zhengzhou 450012, China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Tian
authors.affiliation: Department of Geriatrics, The People's Hospital of Zhengzhou, Zhengzhou 450012, China sunqian166@yeah.net sunqian66@126.com.
authors.forename: Qian
authors.initials: Q
authors.lastname: Sun
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects; D002104:Cadmium / Q000633:toxicity*; D002478:Cells, Cultured; D059865:Endoplasmic Reticulum Stress / Q000187:drug effects* / Q000502:physiology; D004734:Energy Metabolism / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects; D005947:Glucose / Q000378:metabolism; D006706:Homeostasis / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000235:genetics; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D058570:TOR Serine-Threonine Kinases / Q000378:metabolism
chemical_list: D002104:Cadmium; D051057:Proto-Oncogene Proteins c-akt; D058570:TOR Serine-Threonine Kinases; D005947:Glucose
keywords: AKT/mammalian target of rapamycin (mTOR); cadmium toxicity; cardiomyocytes; endoplasmic reticulum (ER) stress; energy metabolism