ArticleAmerican journal of translational research2020
Exacerbating lupus nephritis following BPA exposure is associated with abnormal autophagy in MRL/lpr mice.
Article in American journal of translational research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- ORM1 Mediates Ln-IgG-Induced Podocyte Damage and Autophagy via the AMPK/mTOR Signaling.Organogenesis · 2025Article
- Article
- The spatiotemporal and paradoxical roles of NRF2 in renal toxicity and kidney diseases.Redox biology · 2025Review
- Contributions of Synthetic Chemicals to Autoimmune Disease Development and Occurrence.Current environmental health reports · 2024Review
- LATS2 degradation promoted fibrosis damage and rescued by vitamin K3 in lupus nephritis.Arthritis research & therapy · 2024Article
- Bisphenol A (BPA) and Cardiovascular or Cardiometabolic Diseases.Journal of xenobiotics · 2023Review
- Zinc Deficiency Exacerbates Bisphenol A-Induced Hepatic and Renal Damage: Delineation of Molecular Mechanisms.Biological trace element research · 2023Article
- The Relationship between Typical Environmental Endocrine Disruptors and Kidney Disease.Toxics · 2022Review
- The Potential of Nrf2 Activation as a Therapeutic Target in Systemic Lupus Erythematosus.Metabolites · 2022Review
- Tim-1 alleviates lupus nephritis-induced podocyte injury via regulating autophagy.Central-European journal of immunology · 2021Article
- Potential Mechanisms of Bisphenol A (BPA) Contributing to Human Disease.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
For the development of Lupus nephritis, environmental factors are reasoned to be one of the risk factors. In recent years, the role of bisphenol A (BPA) in kidney injury has attracted wide attention. In this study, we explored the nephrotoxicity and its possible mechanism of BPA exposure to lupus-prone MRL/lpr mice. Orally exposure of BPA increased serum anti-dsDNA level and urinary protein, and aggravated renal pathological injury in MRL/lpr mice. BPA increased the expression of NF-κB protein and activated the inflammatory response in both MRL/lpr and C57 mice. Unlike C57 mice, BPA exposure partially activated autophagy associated proteins, but the autophagy signaling pathway lacked the regulation of Becline1 and LC3-associated phagocytosis deficiency, and decreased Nrf2 protein expression in renal tissue of MRL/lpr mice. Therefore, exacerbating lupus nephritis induced by BPA exposure was associated with the activation of inflammation, abnormal autophagy and decreased antioxidant ability.
Indexed as
Identifiers
32194912PMC7061848W3012705995What 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.