ArticleOncotarget2017
Hyperoside alleviates adriamycin-induced podocyte injury via inhibiting mitochondrial fission.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 34 citations in OpenAlex.
- CCL5 paradoxically regulates glomerular injury by skewing macrophage polarization.JCI insight · 2025Article
- Hyperoside mitigates amphotericin B-induced nephrotoxicity in HK-2 cells via bioenergetic and oxidative stress modulation.BMC pharmacology & toxicology · 2025Article
- The multiple biological activities of hyperoside: from molecular mechanisms to therapeutic perspectives in neoplastic and non-neoplastic diseases.Frontiers in pharmacology · 2025Review
- Hyperoside alleviates myocardial ischemia-reperfusion injury in heart transplantation by promoting mitochondrial fusion via activating the Stat3-Tom70-Opa1 pathway.Frontiers in pharmacology · 2025Article
- Hyperoside ameliorates lupus nephritis by suppressing AKT1-mediated PANoptosis in podocytes: integrating network pharmacology and experimental validation.Frontiers in pharmacology · 2025Article
- [Inhibition of miR-30d-5p promotes mitochondrial autophagy and alleviates high glucose-induced injury in podocytes].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2024Article
- Evaluation of glomerular sirtuin-1 and claudin-1 in the pathophysiology of nondiabetic focal segmental glomerulosclerosis.Scientific reports · 2023Article
- Therapeutic Potential Targeting Podocyte Mitochondrial Dysfunction in Focal Segmental Glomerulosclerosis.Kidney diseases (Basel, Switzerland) · 2023Review
- Article
- Understanding the podocyte immune responses in proteinuric kidney diseases: from pathogenesis to therapy.Frontiers in immunology · 2023Review
- Natural products for kidney disease treatment: Focus on targeting mitochondrial dysfunction.Frontiers in pharmacology · 2023Review
- Flavonoids in Treatment of Chronic Kidney Disease.Molecules (Basel, Switzerland) · 2022Review
- Recent Advances in Traditional Chinese Medicine for Treatment of Podocyte Injury.Frontiers in pharmacology · 2022Review
- The RNA binding protein hnRNPK protects against adriamycin-induced podocyte injury.Annals of translational medicine · 2021Article
- Article
- Mitochondrial Targeting of Herbal Medicine in Chronic Kidney Disease.Frontiers in pharmacology · 2021Review
- MicroRNA-874-3p Aggravates Doxorubicin-Induced Renal Podocyte Injury via Targeting Methionine Sulfoxide Reductase B3.Oxidative medicine and cellular longevity · 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
14 authors at 6 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Podocyte injury underlies many forms of glomerular diseases. Our previous study showed that hyperoside, a naturally occurring flavonoid, could decrease albuminuria at the early stage of diabetic nephropathy by ameliorating renal damage and podocyte injury. However, its protective mechanism against podocyte injury is unknown. A previous study demonstrated that hyperoside might inhibit amyloid β-protein-induced neurotoxicity by suppressing mitochondrial dysfunction. Both mitochondrial dysfunction and its upstream determinant mitochondrial fission were closely related to podocyte injury. Thus, in the current study, we tested the effect of hyperoside on mitochondrial dysfunction and mitochondrial fission in adriamycin (ADR)-induced podocyte injury. In the mice model of ADR-induced nephropathy, hyperoside treatment inhibited ADR-induced albuminuria and podocyte injury. Meanwhile, hyperoside also blocked ADR-induced mitochondrial dysfunction and mitochondrial fission. Consistently, in cultured human podocytes, hyperoside suppressed ADR-induced podocyte injury, mitochondrial dysfunction and mitochondrial fission. All these results indicated that hyperoside might inhibit ADR-induced mitochondrial dysfunction and podocyte injury through suppressing mitochondrial fission both
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.