ArticleMolecular medicine reports2020
Peroxiredoxin I deficiency increases pancreatic β‑cell apoptosis after streptozotocin stimulation via the AKT/GSK3β signaling pathway.
Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Redox Status as a Key Driver of Healthy Pancreatic Beta-Cells.Physiological research · 2024Review
- Effect of peroxiredoxin 1 on the regulation of trophoblast function by affecting autophagy and oxidative stress in preeclampsia.Journal of assisted reproduction and genetics · 2023Article
- Hydrogen peroxide detoxification through the peroxiredoxin/thioredoxin antioxidant system: A look at the pancreatic β-cell oxidant defense.Vitamins and hormones · 2023Article
- Natural COA water inhibits mitochondrial ROS-mediated apoptosis through Plk3 downregulation under STZ diabetic stress in pancreatic β-cell lines.Biochemistry and biophysics reports · 2022Article
- The Role of Thioredoxin/Peroxiredoxin in the β-Cell Defense Against Oxidative Damage.Frontiers in endocrinology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis of pancreatic β‑cells is involved in the pathogenesis of type I and II diabetes. Peroxiredoxin I (Prx I) serves an important role in regulating cellular apoptosis; however, the role of Prx I in pancreatic β‑cell apoptosis is not completely understood. In the present study, the role of peroxiredoxin 1 (Prx I) during streptozotocin (STZ)‑induced apoptosis of pancreatic β‑cells was investigated. The expression level of Prx I was decreased by STZ treatment in a time‑dependent manner, and apoptosis of Prx I knockdown MIN6 cells was increased by STZ stimulation, compared with untransduced MIN6 cells. Furthermore, an intraperitoneal injection of STZ increased pancreatic islet damage in Prx I knockout mice, compared with wild‑type and Prx II knockout mice. AKT and glycogen synthase kinase (GSK)‑3β phosphorylation significantly decreased following Prx I knockdown in MIN6 cells. However, phosphorylated β‑catenin and p65 levels significantly increased after STZ stimulation, compared with untransduced cells. The results of the present study indicate that deletion of Prx I mediated STZ‑induced pancreatic β‑cell death in vivo and in vitro by regulating the AKT/GSK‑3β/β‑catenin signaling pathway, as well as NF‑κB signaling. These findings provide a theoretical basis for treatment of pancreatic damage.
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.