ArticleMolecules (Basel, Switzerland)2016
Renal Protective Effects of 17β-Estradiol on Mice with Acute Aristolochic Acid Nephropathy.
Article in Molecules (Basel, Switzerland), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 31 citations in OpenAlex.
- Sex-specific toxicity targets of aristolochic acids: nephrotoxicity in males, hepatotoxicity in females.Archives of toxicology · 2026Article
- Matricellular protein SMOC2 safeguards tubular integrity in acute kidney injury via integrin β3-dependent inhibition of CCND1-CDK4/6 axis.Molecular biomedicine · 2026Article
- Gender Differences in Adenine Diet-Induced Kidney Toxicity: The Impact of 17β-Estradiol on Renal Inflammation and Fibrosis.International journal of molecular sciences · 2025Article
- Sex differences in the association of long-term exposure to heat stress on kidney function in a large Taiwanese population study.Scientific reports · 2024Article
- Article
- Identification and analysis of differently expressed transcription factors in aristolochic acid nephropathy.Environmental health and preventive medicine · 2024Article
- IL-22 is secreted by proximal tubule cells and regulates DNA damage response and cell death in acute kidney injury.Kidney international · 2024Article
- Article
- Aristolochic acid-induced nephropathy is attenuated in mice lacking the neutral amino acid transporter BAmerican journal of physiology. Renal physiology · 2022Article
- Does Gender Affirming Hormone Therapy Increase the Risk of Kidney Disease?Seminars in nephrology · 2022Review
- Acute and Subchronic Toxicity Studies of Aristolochic Acid A in Tianfu Broilers.Animals : an open access journal from MDPI · 2021Article
- Renoprotective effect ofAmerican journal of physiology. Renal physiology · 2021Article
- Genome-wide transcriptional analysis ofPharmaceutical biology · 2020Article
- Carbon monoxide: An emerging therapy for acute kidney injury.Medicinal research reviews · 2020Review
- Aristolochic Acid-Induced Nephrotoxicity: Molecular Mechanisms and Potential Protective Approaches.International journal of molecular sciences · 2020Review
- Nephrotoxicity of Herbal Medicine and Its Prevention.Frontiers in pharmacology · 2020Review
- Novel kidney dissociation protocol and image-based flow cytometry facilitate improved analysis of injured proximal tubules.American journal of physiology. Renal physiology · 2019Article
- Article
- Effect of phospholipase AThe journal of venomous animals and toxins including tropical diseases · 2018Article
- Agranulocytosis Induced by Sinomenine Hydrochloride.The American journal of case reports · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aristolochic acid nephropathy (AAN) is a progressive kidney disease caused by a Chinese herb containing aristolochic acid. Excessive death of renal tubular epithelial cells (RTECs) characterized the acute phase of AAN. Therapies for acute AAN were limited, such as steroids and angiotensin-receptor blockers (ARBs)/angiotensin-converting enzyme inhibitors (ACEIs). It was interesting that, in acute AAN, female patients showed relative slower progression to renal failure than males. In a previous study, female hormone 17β-estradiol (E2) was found to attenuate renal ischemia-reperfusion injury. Thus, the aim of this study was to investigate the potential protective role of E2 in acute AAN. Compared with male C57BL/6 mice of acute AAN, lower serum creatinine (SCr) and less renal injury, together with RTEC apoptosis in females, were found. Treatment with E2 in male AAN mice reduced SCr levels and attenuated renal tubular injury and RTEC apoptosis. In the mice kidney tissue and human renal proximal tubule cells (HK-2 cells), E2 both attenuated AA-induced cell apoptosis and downregulated the expression of phosphor-p53 (Ser15), p53, and cleaved-caspase-3. This study highlights that E2 exhibited protective effects on the renal injury of acute AAN in male mice by reducing RTEC apoptosis, which might be related to inhibiting the p53 signaling pathway.
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