Hyperglycemia, p53, and mitochondrial pathway of apoptosis are involved in the susceptibility of diabetic models to ischemic acute kidney injury
Open Access
- 1 January 2015
- journal article
- Published by Elsevier BV in Kidney International
- Vol. 87 (1), 137-150
- https://doi.org/10.1038/ki.2014.226
Abstract
No abstract availableThis publication has 50 references indexed in Scilit:
- Tubular p53 Regulates Multiple Genes to Mediate AKIJournal of the American Society of Nephrology, 2014
- Transforming Growth Factor-β–Induced Cross Talk Between p53 and a MicroRNA in the Pathogenesis of Diabetic NephropathyDiabetes, 2013
- Bax and Bak have critical roles in ischemic acute kidney injury in global and proximal tubule–specific knockout mouse modelsKidney International, 2013
- Mitochondrial dynamics: regulatory mechanisms and emerging role in renal pathophysiologyKidney International, 2013
- TNF-α mediates increased susceptibility to ischemic AKI in diabetes.American Journal of Physiology-Renal Physiology, 2013
- p53 Is Renoprotective after Ischemic Kidney Injury by Reducing InflammationJournal of the American Society of Nephrology, 2013
- Vitamin D Receptor Signaling in Podocytes Protects against Diabetic NephropathyJournal of the American Society of Nephrology, 2012
- Mouse model of ischemic acute kidney injury: technical notes and tricksAmerican Journal of Physiology-Renal Physiology, 2012
- Autophagy in proximal tubules protects against acute kidney injuryKidney International, 2012
- Acute kidney injury and chronic kidney disease: an integrated clinical syndromeKidney International, 2012