ArticleKidney research and clinical practice2019
Nrf2-Heme oxygenase-1 modulates autophagy and inhibits apoptosis triggered by elevated glucose levels in renal tubule cells.
Article in Kidney research and clinical practice, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- Sulforaphane regulates hepatic autophagy and apoptosis by modulating Kupffer cells' polarization via Nrf2/HO-1 pathway in the murine hemorrhagic shock/resuscitation model.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2025Article
- Article
- Sulforaphane alleviates renal fibrosis through dual regulation on mTOR-mediated autophagy pathway.International urology and nephrology · 2025Article
- Combination of 10-hydroxy-decanoic acid and ZnO nanoparticles abrogates lead acetate-induced nephrotoxicity in rats: targeting oxidative stress and inflammatory signalling.BMC pharmacology & toxicology · 2025Article
- Hemin protects against cell stress induced by estrogen and progesterone in rat mammary glands via modulation of Nrf2/HO-1 and NF-κB pathways.Cell stress & chaperones · 2023Article
- mtDNA variability determines spontaneous joint aging damage in a conplastic mouse model.Aging · 2022Article
- Conditioned Medium of Adipose-Derived Mesenchymal Stem Cells as a Promising Candidate to Protect High Glucose-Induced Injury in Cultured C28I2 Chondrocytes.Advanced pharmaceutical bulletin · 2022Article
- Blocking REDD1/TXNIP Complex Ameliorates HG-Induced Renal Tubular Epithelial Cell Apoptosis and EMT through Repressing Oxidative Stress.International journal of endocrinology · 2022Article
- ALK7 Knockdown Plays a Protective Role on HG-Stimulated MCs through Activation of the Nrf2/HO-1 Pathway.Disease markers · 2022Article
- Article
- Sulforaphane Inhibits Osteoclastogenesis via Suppression of the Autophagic Pathway.Molecules (Basel, Switzerland) · 2021Article
- Antioxidative Effects ofAntioxidants (Basel, Switzerland) · 2020Article
- cMet agonistic antibody attenuates apoptosis in ischaemia-reperfusion-induced kidney injury.Journal of cellular and molecular medicine · 2020Article
- Role of STAT3/mTOR pathway in chronic kidney injury.American journal of translational research · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAutophagy is a highly balanced process in which lysosomes remove aged and damaged organelles and cellular proteins. Autophagy is essential to maintain homeostasis in the kidneys.
methodsUsing human renal tubule cells HK-2, we assessed the impact of high glucose (HG) on autophagy. We also evaluated the capability of sulforaphane (SFN) to protect the HK-2 cells from HG-induced apoptosis by modulating autophagy.
resultsSFN modulated autophagy and decreased apoptosis in the HK-2 cells that were cultured in 250 mM glucose medium for two days. The reactive oxygen species (ROS) levels increased, as expected, in the cells cultured in the 250 mM glucose medium. However, the SFN decreased the ROS levels in the HK-2 cells. The overexpression of heme oxygenase-1 (HO-1) by SFN decreased the expression of LC3 and beclin-1. LC3 and beclin-1 were involved in the downregulation of caspase-3 that was observed in the HG-induced cells.
conclusionThe activation of nuclear factor E2-related factor 2 (Nrf2)-HO-1 inhibited ROS expression and subsequently attenuated autophagy and cell apoptosis after HG injury was decreased. HG injury led to the activation of autophagy and HO-1 in order to combat oxidative stress and protect against cell apoptosis. Therefore, HO-1 activation can prevent ROS development and oxidative stress during HG injury, which considerably decreases autophagy and apoptosis.
Indexed as
Identifiers
What OpenQuestion holds
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.