Mitochondrial Na + overload is caused by oxidative stress and leads to activation of the caspase 3- dependent apoptotic machinery KUN-TA YANG, SHWU-FEN PAN § , CHUNG-LIANG CHIEN * , SU-MING HSU † , YUNG-ZU TSENG ‡ , SEU-MEI WANG * ,1 and MEI-LIN WU 1 Departments of Physiology and * Anatomy and Cell Biology, College of Medicine, Departments of † Pathology and ‡ Internal Medicine, National Taiwan University Hospital, National Taiwan University, Taipei, Taiwan; and the § Department of Biotechnology, Ming Chuan University, Gwei-Shan, Taoyuan County, Taiwan 1 Correspondence: Department of Physiology (M.-L.W.) and Department of Anatomy and Cell Biology (S.-M.W), College of Medicine, National Taiwan University, No. 1, Sec. 1, Jen-Ai Rd., Taipei, Taiwan. E-mail: mlw@ha.mc.ntu.edu.tw <h3>SPECIFIC AIMS</h3> In many cell types, oxidative stress and mitochondrial Ca 2+ ([Ca] m ) overload lead to the opening of the permeability transition pore (PTP), resulting in persistent loss of mitochondrial potential (Δϕ m ), cytochrome c (cytC) release, and apoptosis. We used treatment with H 2 O 2 , a widely accepted model system for studying oxidative stress-induced apoptosis in many cell types and in cardiovascular disease. Using time-lapse confocal recording of live cardiomyocytes, we found that H
End of preview. The entire article is 3 pages. To view the full-text, please rent this article to continue.
/lp/fed-of-american-socs-for-experimental-biology/mitochondrial-na-overload-is-caused-by-oxidative-stress-and-leads-to-MyAUOMWXJ8
Welcome to DeepDyve! Rent Premier Research Articles and Save Up to 90%
Mitochondrial Na+ overload is caused by oxidative stress and leads to activation of the caspase 3- dependent apoptotic machinery
YANG, KUN-TA; PAN, SHWU-FEN; CHIEN, CHUNG-LIANG; HSU, SU-MING; TSENG, YUNG-ZU; WANG, SEU-MEI; WU, MEI-LIN
Follow The FASEB Journal
, Volume 18 (12): 1442
Fed of American Socs for Experimental Biology – Sep 1, 2004
More Info
More Like This Article
View All dataSource[]=actageo&dataSource[]=aspet&dataSource[]=aaos&dataSource[]=aacc&dataSource[]=aacr&dataSource[]=aea&dataSource[]=aip&dataSource[]=ajnr&dataSource[]=ams&dataSource[]=aps_physical&dataSource[]=appi_book&dataSource[]=appi_journal&dataSource[]=apha&dataSource[]=asip&dataSource[]=asm&dataSource[]=asn&dataSource[]=aspb&dataSource[]=avs&dataSource[]=annual_reviews&dataSource[]=arxiv&dataSource[]=acm&dataSource[]=berghahn&dataSource[]=cabi&dataSource[]=clinical_trials&dataSource[]=dailymed&dataSource[]=degruyter&dataSource[]=du_press&dataSource[]=esa&dataSource[]=eu_press&dataSource[]=elsevier&dataSource[]=emerald&dataSource[]=ejtr&dataSource[]=emea&dataSource[]=epo&dataSource[]=faseb&dataSource[]=gsa&dataSource[]=health_affairs&dataSource[]=hindawi&dataSource[]=imanager&dataSource[]=imedpub&dataSource[]=informa_healthcare&dataSource[]=informs&dataSource[]=iop&dataSource[]=iucr&dataSource[]=iospress&dataSource[]=jbjs&dataSource[]=leftcoast&dataSource[]=lu_press&dataSource[]=mesharpe&dataSource[]=mary_ann_liebert&dataSource[]=medline&dataSource[]=mit_press&dataSource[]=nature&dataSource[]=oxford&dataSource[]=pier_professional&dataSource[]=pnas&dataSource[]=portlandpress&dataSource[]=psyc_articles&dataSource[]=psyc_books&dataSource[]=psyc_critiques&dataSource[]=plos_journal&dataSource[]=pubmed_central&dataSource[]=rsna&dataSource[]=rockefeller&dataSource[]=rcn&dataSource[]=ria&dataSource[]=rsc&dataSource[]=sage&dataSource[]=spie&dataSource[]=springer_journal&dataSource[]=springer&dataSource[]=taylor_francis&dataSource[]=aps&dataSource[]=the_scientist&dataSource[]=uc_press&dataSource[]=uspto_abstract&dataSource[]=wiley&dataSource[]=pct
© 2012 DeepDyve, Inc. All rights reserved.
Terms of Service | Privacy Policy
