ArticleAmerican journal of physiology. Renal physiology2013
mTOR plays a critical role in p53-induced oxidative kidney cell injury in HIVAN.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- PKR activation-induced mitochondrial dysfunction in HIV-transgenic mice with nephropathy.eLife · 2024Article
- ROS Chronicles in HIV Infection: Genesis of Oxidative Stress, Associated Pathologies, and Therapeutic Strategies.Current issues in molecular biology · 2024Review
- Autophagy attenuates high glucose-induced oxidative injury to lens epithelial cells.Bioscience reports · 2020Article
- Modulation of mTORC1 Signaling Pathway by HIV-1.Cells · 2020Review
- Metabolic pathway activation distinguishes transcriptional signatures of CD8+ T cells from HIV-1 elite controllers.AIDS (London, England) · 2018Article
- Polyploidy and Mitotic Cell Death Are Two Distinct HIV-1 Vpr-Driven Outcomes in Renal Tubule Epithelial Cells.Journal of virology · 2018Article
- tRNA fragmentation and protein translation dynamics in the course of kidney injury.RNA biology · 2018Review
- Molecular Mechanisms of Proteinuria in Focal Segmental Glomerulosclerosis.Frontiers in medicine · 2018Review
- Molecular Mechanisms of Injury in HIV-Associated Nephropathy.Frontiers in medicine · 2018Review
- Roles of mTOR complexes in the kidney: implications for renal disease and transplantation.Nature reviews. Nephrology · 2016Review
- Impact of APOL1 polymorphism and IL-1β priming in the entry and persistence of HIV-1 in human podocytes.Retrovirology · 2016Article
- Coexpression Network Analysis of Benign and Malignant Phenotypes of SIV-Infected Sooty Mangabey and Rhesus Macaque.PloS one · 2016Article
- HIV-associated nephropathies: epidemiology, pathology, mechanisms and treatment.Nature reviews. Nephrology · 2015Review
- Interactions between Myc and Mediators of Inflammation in Chronic Liver Diseases.Mediators of inflammation · 2015Review
- Renin angiotensin system modulates mTOR pathway through AT2R in HIVAN.Experimental and molecular pathology · 2014Article
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
Oxidative stress has been implicated to contribute to HIV-induced kidney cell injury; however, the role of p53, a modulator of oxidative stress, has not been evaluated in the development of HIV-associated nephropathy (HIVAN). We hypothesized that mammalian target of rapamycin (mTOR) may be critical for the induction of p53-mediated oxidative kidney cell injury in HIVAN. To test our hypothesis, we evaluated the effect of an mTOR inhibitor, rapamycin, on kidney cell p53 expression, downstream signaling, and kidney cell injury in both in vivo and in vitro studies. Inhibition of the mTOR pathway resulted in downregulation of renal tissue p53 expression, associated downstream signaling, and decreased number of sclerosed glomeruli, tubular microcysts, and apoptosed and 8-hydroxy deoxyguanosine (8-OHdG)-positive (+ve) cells in Tg26 mice. mTOR inhibition not only attenuated kidney cell expression of p66ShcA and phospho-p66ShcA but also reactivated the redox-sensitive stress response program in the form of enhanced expression of manganese superoxide dismutase (MnSOD) and catalase. In in vitro studies, the mTOR inhibitor also provided protection against HIV-induced podocyte apoptosis. Moreover, mTOR inhibition downregulated HIV-induced podocyte (HP/HIV) p53 expression. Since HP/HIV silenced for mTOR displayed a lack of expression of p53 as well as attenuated podocyte apoptosis, this suggests that mTOR is critical for kidney cell p53 activation and associated oxidative kidney cell injury in the HIV milieu.
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