Ecotoxicology and environmental safety · 2025
Unraveling the molecular mechanisms underlying environmental benzophenone-3 exposure and chronic kidney disease.
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Wu Xiangyan, Tan Ziyi, Chen Hankun, Liu Yirui, Zhu Wei, Zhao Yao, Zhou Yang
Аннотация
BACKGROUND: Benzophenone-3 (BP-3), a commonly used ultraviolet filter and stabilizer in commercial products, has raised concern due to its potential adverse health effects. This study aims to explore the potential association between BP-3 and chronic kidney disease (CKD) and to identify key genes that may play a critical bridging role in this process.
METHODS: To clarify the relationship between BP-3 exposure and chronic kidney disease (CKD), this study employed an integrative strategy combining network toxicology, non-negative matrix factorization, machine learning algorithms, and molecular simulations.
RESULTS: Our analysis identified a group of BP-3-associated CKD pathogenic genes that are enriched in inflammatory and metabolic pathways. We further uncovered two distinct CKD subtypes: C1 (inflammation-dominant) and C2 (metabolism-dominant), each displaying unique molecular profiles. Among the candidate genes, three hub genes, CX3CR1, CXCR4, and CCR1, were pinpointed as central players. Molecular docking and dynamics simulations provided additional evidence, confirming that BP-3 can bind directly and stably to the proteins encoded by these hub genes.
CONCLUSION: These results demonstrate that BP-3-associated CKD is mediated by a complex interplay between inflammatory and metabolic pathways. Our findings not only offer novel mechanistic insights into how environmental pollutants contribute to CKD pathogenesis but also highlight potential targets for future risk assessment and preventive strategies.
METHODS: To clarify the relationship between BP-3 exposure and chronic kidney disease (CKD), this study employed an integrative strategy combining network toxicology, non-negative matrix factorization, machine learning algorithms, and molecular simulations.
RESULTS: Our analysis identified a group of BP-3-associated CKD pathogenic genes that are enriched in inflammatory and metabolic pathways. We further uncovered two distinct CKD subtypes: C1 (inflammation-dominant) and C2 (metabolism-dominant), each displaying unique molecular profiles. Among the candidate genes, three hub genes, CX3CR1, CXCR4, and CCR1, were pinpointed as central players. Molecular docking and dynamics simulations provided additional evidence, confirming that BP-3 can bind directly and stably to the proteins encoded by these hub genes.
CONCLUSION: These results demonstrate that BP-3-associated CKD is mediated by a complex interplay between inflammatory and metabolic pathways. Our findings not only offer novel mechanistic insights into how environmental pollutants contribute to CKD pathogenesis but also highlight potential targets for future risk assessment and preventive strategies.