ArticleToxins2020
Therapeutic Targeting of Aristolochic Acid Induced Uremic Toxin Retention, SMAD 2/3 and JNK/ERK Pathways in Tubulointerstitial Fibrosis: Nephroprotective Role of Propolis in Chronic Kidney Disease.
Article in Toxins, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Trial
- Effects of Propolis Supplementation on Gut Microbiota and Uremic Toxin Profiles of Patients Undergoing Hemodialysis.Toxins · 2024Trial
- Evaluation of the Antioxidant Properties and Biological Effects of a Novel Combined Barberry Root-Propolis Extract on HEK293T Cells.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Propolis and its therapeutic effects on renal diseases: A review.Iranian journal of basic medical sciences · 2024Review
- The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023Review
- Novel Approaches in Chronic Renal Failure without Renal Replacement Therapy: A Review.Biomedicines · 2023Review
- Protein-Bound Uremic Toxins in Senescence and Kidney Fibrosis.Biomedicines · 2023Review
- Propolis and Their Active Constituents for Chronic Diseases.Biomedicines · 2023Review
- Jiangtang Decoction Ameliorates Diabetic Kidney Disease Through the Modulation of the Gut Microbiota.Diabetes, metabolic syndrome and obesity : targets and therapy · 2023Article
- Crosstalk between proximal tubular epithelial cells and other interstitial cells in tubulointerstitial fibrosis after renal injury.Frontiers in endocrinology · 2023Review
- Enterorenal crosstalks in diabetic nephropathy and novel therapeutics targeting the gut microbiota.Acta biochimica et biophysica Sinica · 2022Review
- Molecular Mechanistic Pathways Targeted by Natural Antioxidants in the Prevention and Treatment of Chronic Kidney Disease.Antioxidants (Basel, Switzerland) · 2021Review
- Article
- Propolis in Metabolic Syndrome and Its Associated Chronic Diseases: A Narrative Review.Antioxidants (Basel, Switzerland) · 2021Review
- c-Jun Amino Terminal Kinase Signaling Promotes Aristolochic Acid-Induced Acute Kidney Injury.Frontiers in physiology · 2021Article
- Two New Aristolochic Acid Analogues from the Roots ofMolecules (Basel, Switzerland) · 2020Article
Corrections and comments
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Authors and funding
9 authors at 7 institutions in 1 country.
Funding
Abstract
The nephrotoxicity of aristolochic acids (AAs), p-cresyl sulfate (PCS) and indoxyl sulfate (IS) were well-documented, culminating in tubulointerstitial fibrosis (TIF), advanced chronic kidney disease (CKD) and fatal urothelial cancer. Nonetheless, information regarding the attenuation of AAs-induced nephropathy (AAN) and uremic toxin retention is scarce. Propolis is a versatile natural product, exerting anti-oxidant, anti-cancer and anti-fibrotic properties. We aimed to evaluate nephroprotective effects of propolis extract (PE) in a murine model. AAN was developed to retain circulating PCS and IS using C57BL/6 mice, mimicking human CKD. The kidney sizes/masses, renal function indicators, plasma concentrations of PCS/IS, tissue expressions of TIF, α-SMA, collagen IaI, collagen IV and signaling pathways in transforming growth factor-β (TGF-β) family were analyzed among the control, PE, AAN, and AAN-PE groups. PE ameliorated AAN-induced renal atrophy, renal function deterioration, TIF, plasma retention of PCS and IS. PE also suppressed α-SMA expression and deposition of collagen IaI and IV in the fibrotic epithelial-mesenchymal transition. Notably, PE treatment in AAN model inhibited not only SMAD 2/3-dependent pathways but also SMAD-independent JNK/ERK activation in the signaling cascades of TGF-β family. Through disrupting fibrotic epithelial-mesenchymal transition and TGF-β signaling transduction pathways, PE improves TIF and thereby facilitates renal excretion of PCS and IS in AAN. In light of multi-faced toxicity of AAs, PE may be capable of developing a new potential drug to treat CKD patients exposed to AAs.
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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.