Reticulon-1A mediates diabetic kidney disease progression through endoplasmic reticulum-mitochondrial contacts in tubular epithelial cells
- 22 April 2022
- journal article
- research article
- Published by Elsevier in Kidney International
- Vol. 102 (2) , 293-306
Abstract
No abstract availableKeywords
Funding Information
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (P01DK56492, R01DK109683, R01DK122980, R01DK129467)
- U.S. Department of Veterans Affairs (/ NIDDK R01DK117913-01, I01BX000345)
This publication has 49 references indexed in Scilit:
- Can We Target Tubular Damage to Prevent Renal Function Decline in Diabetes?Seminars in Nephrology, 2012
- PERK is required at the ER-mitochondrial contact sites to convey apoptosis after ROS-based ER stressCell Death & Differentiation, 2012
- Hexokinase regulates Bax-mediated mitochondrial membrane injury following ischemic stressKidney International, 2011
- The endoplasmic reticulum stress response and diabetic kidney diseaseAmerican Journal of Physiology-Renal Physiology, 2011
- Endoplasmic reticulum stress in proteinuric kidney diseaseKidney International, 2010
- Proteinuria and Hyperglycemia Induce Endoplasmic Reticulum StressJournal of the American Society of Nephrology, 2008
- Regulation of hexokinase binding to VDACJournal of Bioenergetics and Biomembranes, 2008
- Histopathology of Diabetic NephropathySeminars in Nephrology, 2007
- Testosterone promotes apoptotic damage in human renal tubular cellsKidney International, 2004
- Mitochondrial Binding of Hexokinase II Inhibits Bax-induced Cytochrome c Release and ApoptosisJournal of Biological Chemistry, 2002