Bisphenol A, an environmental estrogen-like toxic chemical, induces cardiac fibrosis by activating the ERK1/2 pathway
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- 作者：Yingying Hua ; b ; 1 ; Li Zhangc ; 1 ; Xianxian Wua ; 1 ; Liangyu Houa ; Zhange Lia ; Jin Jua ; Qian Lid ; Wei Qina ; Jiamin Lia ; Qingwei Zhanga ; Tong Zhoua ; Longyin Zhanga ; Chaoqian Xua ; Zhiwei Fanga ; Yong Zhanga ; e ; f ; hmuzhangyong@hotmail.com" class="auth_mail" title="E-mail the corresponding author ; zy@ems.hrbmu.edu.cn" class="auth_mail" title="E-mail the corresponding author
- 关键词：BPA ; bisphenol A ; EF ; ejection fraction ; ECM ; extracellular matrix ; ER ; estrogen receptor ; ERK1/2 ; extracellular signal-regulated kinase 1/2 ; FS ; fractional shortening ; GPER ; G protein-coupled receptor ; IVS ; interventricular septum ; JNK ; c-Jun N-terminal kinase ; LVID ; left ventricular internal dimension ; LVPW ; left ventricular posterior wall ; MAPK ; mitogen-activated protein kinase ; TGF-β1 ; transforming growth factor-β1
- 刊名：Toxicology Letters
- 出版年：2016
- 出版时间：27 May 2016
- 年：2016
- 卷：250-251
- 期：Complete
- 页码：1-9
- 全文大小：2759 K
文摘
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Exposure to a high dosage of bisphenol A (BPA) comparable to its urinary concentration decreased cardiac function.
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BPA induced cardiac fibrosis.
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BPA markedly facilitated proliferation and collagen production of cardiac fibroblasts by activating ERK1/2.
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Antiestrogen or ERK inhibitor prevented BPA-induced proliferation and collagen production of cardiac fibroblasts, indicating that BPA acts by activating estrogen receptor and the ERK1/2-dependent pathways.