ArticleAging2023
Article in Aging, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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.
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.
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Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Dendrobium officinale polysaccharide ameliorate hyperlipidemia through LKB1/AMPK and CD36/PGC-1α/UCP1 activation and gut microbiota modulation.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The role of TOMM20 in Mediating TERT translocation to mitochondria and its impact on mitophagy in membranous nephropathy.BMC nephrology · 2026Article
- Dendrobium officinale polysaccharides alleviate atopic dermatitis in vivo and in vitro through inhibition of inflammation and mitochondrial dysfunction.Journal of molecular histology · 2026Article
- Integrated metabolomics and computational analysis suggest that aFrontiers in nutrition · 2026Article
- SP1 activates AKT3 to facilitate the development of diabetic nephropathy.Journal of endocrinological investigation · 2025Article
- Important regulatory role of mitophagy in diabetic microvascular complications.Journal of translational medicine · 2025Review
- Protective effect of compound K against podocyte injury in chronic kidney disease by maintaining mitochondrial homeostasis.Scientific reports · 2025Article
- Inhibition of retinal neovascularization by Dendrobium polysaccharides: a review.Frontiers in pharmacology · 2025Review
- Research progress on the regulatory and pharmacological mechanism of chemical components of Dendrobium.Heliyon · 2024Review
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
backgroundsHigh glucose (HG) caused oxidative stress and mitochondrial dysfunction, resulting in insulin resistance in podocytes, a key mechanism of diabetic nephropathy.
objectiveThe purpose of this study is to explore the mechanism by which DOP decreases the podocyte injury induced by HG.
methodsMPC5 cells were treated with HG, DOP, and IRS-1/2 inhibitor NT157. Afterwards, glucose consumption, generations of ROS and MDA were measured using the detection kits. Mitophagy was monitored using both MtphagTracyker and LysoTracker. The mitochondrial membrane potential was evaluated by JC-1 staining. DOP was also used in a mouse model of diabetes, with the measurements of urine albumin, blood creatinine and blood urea nitrogen.
resultsTreatment with DOP suppressed the HG-induced reduction of glucose consumption, the phosphorylation of IRS-1 (phospho Y632), AKT (phospho Ser473 and Thr308) and Nephrin. In addition, HG-induced augment of ROS and MDA, formation of γ-H2A.X foci and translocation of AKT to nucleus were inhibited by DOP. DOP enhanced mitophagy, which was associated with decreased mitochondrial membrane potential and ROS production. DOP conferred protective effect on podocyte in the diabetic mouse by reducing the albumin/creatinine ratio and blood urea nitrogen, and restoring Nephrin expression in podocytes.
conclusionsDOP alleviates HG-induced podocyte injuryby regulating IRS-1/AKT signal and promoting mitophagy.
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What Socratic 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 Socratic graph.