ArticleAmerican journal of physiology. Renal physiology2013
Aquaporin 11 insufficiency modulates kidney susceptibility to oxidative stress.
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 24 papers.
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Who cites it
24 citing papers in PubMed, 49 citations in OpenAlex.
- A pan-vertebrate signaling motif controls the molecular function of intracellular AQP12.The Journal of cell biology · 2026Article
- Cryo-EM structure of human AQP11 reveals a trimeric architecture with a large pore.Science advances · 2026Article
- Regulation of renal aquaporins: implications in tubular epithelial integrity.Biochemical Society transactions · 2026Review
- Peroxiporins and Oxidative Stress: Promising Targets to Tackle Inflammation and Cancer.International journal of molecular sciences · 2024Review
- Protective roles of peroxiporins AQP0 and AQP11 in human astrocyte and neuronal cell lines in response to oxidative and inflammatory stressors.Bioscience reports · 2024Article
- The therapeutic prospect of zinc oxide nanoparticles in experimentally induced diabetic nephropathy.Tissue barriers · 2023Article
- Aquaporin Gating: A New Twist to Unravel Permeation through Water Channels.International journal of molecular sciences · 2022Review
- Abnormal expression and the significant prognostic value of aquaporins in clear cell renal cell carcinoma.PloS one · 2022Article
- A Cardioplegic Solution with an Understanding of a Cardiochannelopathy.Antioxidants (Basel, Switzerland) · 2021Review
- The Vanderbilt O'Brien Kidney Center.American journal of physiology. Renal physiology · 2021Review
- Hydrogen peroxide in the ER: A tale of triage.Redox biology · 2020Article
- The ER-localized aquaporin SIP2;1 is involved in pollen germination and pollen tube elongation in Arabidopsis thaliana.Plant molecular biology · 2019Article
- miR-27b-mediated suppression of aquaporin-11 expression in hepatocytes reduces HCV genomic RNA levels but not viral titers.Virology journal · 2019Article
- Aquaporin Channels in the Heart-Physiology and Pathophysiology.International journal of molecular sciences · 2019Review
- Peroxiporins in Cancer.International journal of molecular sciences · 2019Review
- Involvement of the NADPH oxidase 2 pathway in renal oxidative stress inBiochemistry and biophysics reports · 2019Article
- Aquaporins in Renal Diseases.International journal of molecular sciences · 2019Review
- Regulation of Aquaporin Functional Properties Mediated by the Antioxidant Effects of Natural Compounds.International journal of molecular sciences · 2017Article
- Aquaporin-Mediated Water and Hydrogen Peroxide Transport Is Involved in Normal Human Spermatozoa Functioning.International journal of molecular sciences · 2016Article
- Aquaporin 11, a regulator of water efflux at retinal Müller glial cell surface decreases concomitant with immune-mediated gliosis.Journal of neuroinflammation · 2016Article
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Authors and funding
20 authors at 5 institutions in 2 countries.
Funding
Abstract
Aquaporin 11 (AQP11) is a newly described member of the protein family of transport channels. AQP11 associates with the endoplasmic reticulum (ER) and is highly expressed in proximal tubular epithelial cells in the kidney. Previously, we identified and characterized a recessive mutation of the highly conserved Cys227 to Ser227 in mouse AQP11 that caused proximal tubule (PT) injury and kidney failure in mutant mice. The current study revealed induction of ER stress, unfolded protein response, and apoptosis as molecular mechanisms of this PT injury. Cys227Ser mutation interfered with maintenance of AQP11 oligomeric structure. AQP11 is abundantly expressed in the S1 PT segment, a site of major renal glucose flux, and Aqp11 mutant mice developed PT-specific mitochondrial injury. Glucose increased AQP11 protein expression in wild-type kidney and upregulation of AQP11 expression by glucose in vitro was prevented by phlorizin, an inhibitor of sodium-dependent glucose transport across PT. Total AQP11 levels in heterozygotes were higher than in wild-type mice but were not further increased in response to glucose. In Aqp11 insufficient PT cells, glucose potentiated increases in reactive oxygen species (ROS) production. ROS production was also elevated in Aqp11 mutation carriers. Phenotypically normal mice heterozygous for the Aqp11 mutation repeatedly treated with glucose showed increased blood urea nitrogen levels that were prevented by the antioxidant sulforaphane or by phlorizin. Our results indicate an important role for AQP11 to prevent glucose-induced oxidative stress in proximal tubules.
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