Caspase-3 activation in addition to a decreased number of TUNEL-positive cells. Moreover, opening of mitochondrial KATP channels by POC could play a pivotalORIGINAL ARTICLEPostconditioning attenuates mitochondrial damagerole in stopping oxidative pressure and attenuating mtDNA damage in renal I/R injury. We conclude that POC might be a promising therapy for protection against I/R injury.AC K N O W L E D G E M E N T S This operate was supported by National Natural Science Foundation of China Award number 30900591 and Plan of New Century Outstanding Talents of Ministry of Education in China, Award quantity NCET-10-0448.C O N F L I C T O F I N T E R E S T S TAT E M E N T None declared. (See related article by Moradi and Wang. Renoprotective mechanisms of ischemic postconditioning in ischemiareperfusion injury: improved mitochondrial function and integrity. Nephrol Dial Transplant 2013; 28: 2667669.)
HHS Public AccessAuthor manuscriptNature. Author manuscript; accessible in PMC 2014 April 17.Published in final edited type as: Nature. 2013 October 17; 502(7471): 37780. doi:ten.1038/nature12508.Author Manuscript Author Manuscript Author Manuscript Author ManuscriptA statin-dependent QTL for GATM CCR1 Source expression is linked with statin-induced myopathyLara M. Mangravite1,, Barbara E. Engelhardt2,12,, Marisa W. Medina3, Joshua D. Smith4, Christopher D. Brown5, Daniel I. Chasman6, Brigham H. Mecham1, Bryan Howie2, Gap Junction Protein site Heejung Shim2, Devesh Naidoo3, QiPing Feng7, Mark J. Rieder4,13, Y-D I. Chen8, Jerome I. Rotter8, Paul M. Ridker6, Jemma C. Hopewell9, Sarah Parish9, Jane Armitage9, Rory Collins9, Russell A. Wilke7, Deborah A. Nickerson4, Matthew Stephens2,ten,11, and Ronald M. Krauss3,1SageBionetworks, Seattle, Washington, USA of Human Genetics, University of Chicago, Chicago, Illinois, USA2Department 3Children’sHospital Oakland Investigation Institute, Oakland, California, USA of Genome Sciences, University of Washington, Seattle, Washington, USA of Genetics, University of Pennsylvania, Philadelphia, PA4Department 5Department 6Centerfor Cardiovascular Illness Prevention, Division of Preventative Medicine, Brigham and Women’s Hospital, Boston, MA7Departmentof Medicine, Division of Clinical Pharmacology, Vanderbilt University Medical Center, Nashville, TN, USA Genetics Institute, Cedars-Sinai, Los Angeles, CA8MedicalUsers may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, topic generally towards the full Conditions of use:http://nature/authors/editorial_policies/license.html#terms Correspondence should be addressed to: L.M.M. ([email protected]), M.S. ([email protected]), or R.M.K. ([email protected]). These authors contributed equally to this function. 11These authors co-directed this project. 12Current Address: Biostatistics and Bioinformatics Division and Department of Statistical Science, Duke University, Durham, NC, USA 13Current Address: Adaptive Biotechnologies, Seattle, WA, USA. Author Contributions L.M.M. developed experiment and analyses, generated samples, performed analyses, and wrote the manuscript. B.E.E. developed and performed analyses and wrote the manuscript. C.D.B. performed analyses of ENCODE information. B.H.M. designed and performed correlation analyses. J.D.S., M.J.R., and D.A.N. generated expression and genotype information. M.W.M. and D.N. created, performed and analyzed functional experiments. B.H. and H.S. developed and performed the imputation methodology, R.A.W, Q.F, J.D.S, M.J.R. and D.