ArticleOxidative medicine and cellular longevity2020
Overexpression of miR-506-3p Aggravates DBP-Induced Testicular Oxidative Stress in Rats by Downregulating ANXA5 via Nrf2/HO-1 Signaling Pathway.
Article in Oxidative medicine and cellular longevity, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 1 of them a synthesis that pooled it.
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Who cites it
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- A Systematic Literature Review of Reproductive Toxicological Studies on Phthalates.International journal of molecular sciences · 2025Pooled it
- Dibutyl phthalate exposure induces thyroid toxicity through follicular cell pyroptosisAnnals of medicine · 2026Article
- Protective effects of 20(R) ginsenoside Rg3 on DBP-induced reproductive injury in mice through Nrf2/ARE pathway.Scientific reports · 2025Article
- Dysregulation of microRNA (miRNA) Due to Phthalate/Phthalate Metabolite Exposure and Associated Health Effects: A Narrative Review.Journal of xenobiotics · 2025Review
- Phthalates toxicityHeliyon · 2025Article
- ANXA5: related mechanisms of osteogenesis and additional biological functions.Frontiers in cell and developmental biology · 2025Review
- Identifying Oxidized Lipid Metabolism-Related LncRNAs as Prognostic Biomarkers of Head and Neck Squamous Cell Carcinoma.Journal of personalized medicine · 2023Article
- Knockdown of circ_0003928 ameliorates high glucose-induced dysfunction of human tubular epithelial cells through the miR-506-3p/HDAC4 pathway in diabetic nephropathy.European journal of medical research · 2022Article
- Integrative proteomics and m6A microarray analyses of the signatures induced by METTL3 reveals prognostically significant in gastric cancer by affecting cellular metabolism.Frontiers in oncology · 2022Article
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Authors and funding
8 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
backgroundDi-N-butylphthalate (DBP) is a kind of unique endocrine toxicity linked to hormonal disruptions that affects the male reproductive system and has given rise to more and more attention. However, the mechanism of DBP-induced testicular injury remains unclear. Here, the objective of this study was to investigate the potential molecular mechanism of miR-506-3p in DBP-induced rat testicular oxidative stress injury via ANXA5 (Annexin A5)/Nrf2/HO-1 signaling pathway.
methods
resultsDifferentially expressed miRNAs between the DBP-treated and normal rats were analyzed, and qRT-PCR showed miR-506-3p was highly expressed in testicular tissues of the DBP-treated rats. DBP-treated rats presented severe inflammatory infiltration, increased abnormal germ cells, and missed cell layers frequently existed in seminiferous tubules, resulted in oxidative stress and decreased testicular function. Meanwhile, upregulation of miR-506-3p aggravated the above changes. In addition, miR-506-3p directly bound to ANXA5, and overexpression of miR-506-3p could reduce the ANXA5 expression and also decrease the protein levels of Nrf2/HO-1 signaling pathway. Additionally, we found that recombinant rat ANXA5 reversed the DBP-treated testicular oxidative stress promoting injury of miR-506-3p in rats.
conclusionsThis study provided evidence that miR-506-3p could aggravate the DBP-treated testicular oxidative stress injury
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