ArticleFree radical biology & medicine2012
NAD(P)H:quinone oxidoreductase 1 protects bladder epithelium against painful bladder syndrome in mice.
Article in Free radical biology & medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
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- Nrf2 Pathway Ameliorates Bladder Dysfunction in Cyclophosphamide-Induced Cystitis via Suppression of Oxidative Stress.Oxidative medicine and cellular longevity · 2021Article
- The Inhibitory Effects of Cobalt Protoporphyrin IX and Cannabinoid 2 Receptor Agonists in Type 2 Diabetic Mice.International journal of molecular sciences · 2017Article
- The induction of the transcription factor Nrf2 enhances the antinociceptive effects of delta-opioid receptors in diabetic mice.PloS one · 2017Article
- Data on bone marrow stem cells delivery using porous polymer scaffold.Data in brief · 2016Article
- Melatonin inhibits manganese-induced motor dysfunction and neuronal loss in mice: involvement of oxidative stress and dopaminergic neurodegeneration.Molecular neurobiology · 2015Article
Corrections and comments
- Correction · 2014-12-01Error in Image · Unreliable Image ·
- Erratum issued
- Erratum issued
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Painful bladder syndrome (PBS), or interstitial cystitis, is a poorly understood chronic disease that is characterized by thinning of the bladder epithelium and intense pain. Here we demonstrate that NAD(P)H:quinone oxidoreductase 1(-/-) (NQO1(-/-)) mice developed in our laboratory represent a new animal model of PBS. NQO1 is known to protect against physiological stress as well as protecting transcription factors against proteasomal degradation. In this study we demonstrate that NQO1 is necessary for bladder epithelium integrity and to prevent the development/progression of PBS. We observed downregulation of energy metabolism, adhesion, and apoptotic signaling cascades, which led to mitochondrial aberrations and profound alterations in energy metabolism, increased susceptibility to reactive oxygen species generation, and apoptosis in luminal epithelium in NQO1(-/-) mice that were absent in wild-type mice. These pathophysiological changes led to the incidence of PBS in NQO1(-/-) mice. Altogether, the results demonstrate for the first time that NQO1 is an endogenous factor in protection against PBS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.