Deficiency of aldehyde dehydrogenase 2 aggravates ethanol-induced cytotoxicity in N2a cells via CaMKII/Drp1-mediated mitophagy

Yan, Tingting; Chen, Jiyang; Wang, Yalin; Wang, Yinuo; Zhang, Yuanqingzhi; Zhao, Yan

doi:10.1016/j.fct.2023.114129

Food and Chemical Toxicology

2023

DOI: 10.1016/j.fct.2023.114129

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Deficiency of aldehyde dehydrogenase 2 aggravates ethanol-induced cytotoxicity in N2a cells via CaMKII/Drp1-mediated mitophagy

Tingting Yan,

Jiyang Chen,

Yalin Wang

et al.

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2024

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Cited by 2 publications

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Environmental endocrine disrupting chemical 4-tert-butylphenol induced calcium overload and subsequent autophagy impairment via miRNA-363/CACNA1D Axis in epithelioma papulosum cyprini cells

Cui,

Liang,

Liu

et al. 2024

Comparative Biochemistry and Physiology Part C: Toxicology &

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Environmental endocrine disrupting chemical 4-tert-butylphenol induced calcium overload and subsequent autophagy impairment via miRNA-363/CACNA1D Axis in epithelioma papulosum cyprini cells

Cui,

Liang,

Liu

et al. 2024

Comparative Biochemistry and Physiology Part C: Toxicology &

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Dexmedetomidine ameliorates acute kidney injury by regulating mitochondrial dynamics via the α2-AR/SIRT1/PGC-1α pathway activation in rats

Zhang,

Feng,

Yang

et al. 2024

Mol Med

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Background Sepsis-associated acute kidney injury (AKI) is a serious complication of systemic infection with high morbidity and mortality in patients. However, no effective drugs are available for AKI treatment. Dexmedetomidine (DEX) is an alpha 2 adrenal receptor agonist with antioxidant and anti-apoptotic effects. This study aimed to investigate the therapeutic effects of DEX on sepsis-associated AKI and to elucidate the role of mitochondrial dynamics during this process. Methods A lipopolysaccharide (LPS)-induced AKI rat model and an NRK-52E cell model were used in the study. This study investigated the effects of DEX on sepsis-associated AKI and the molecular mechanisms using histologic assessment, biochemical analyses, ultrastructural observation, western blotting, immunofluorescence, immunohistochemistry, qRT-PCR, flow cytometry, and si-mRNA transfection. Results In rats, the results showed that administration of DEX protected kidney structure and function from LPS-induced septic AKI. In addition, we found that DEX upregulated the α2-AR/SIRT1/PGC-1α pathway, protected mitochondrial structure and function, and decreased oxidative stress and apoptosis compared to the LPS group. In NRK-52E cells, DEX regulated the mitochondrial dynamic balance by preventing intracellular Ca2+ overloading and activating CaMKII. Conclusions DEX ameliorated septic AKI by reducing oxidative stress and apoptosis in addition to modulating mitochondrial dynamics via upregulation of the α2-AR/SIRT1/PGC-1α pathway. This is a confirmatory study about DEX pre-treatment to ameliorate septic AKI. Our research reveals a novel mechanistic molecular pathway by which DEX provides nephroprotection.

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Deficiency of aldehyde dehydrogenase 2 aggravates ethanol-induced cytotoxicity in N2a cells via CaMKII/Drp1-mediated mitophagy

Cited by 2 publications

References 46 publications

Environmental endocrine disrupting chemical 4-tert-butylphenol induced calcium overload and subsequent autophagy impairment via miRNA-363/CACNA1D Axis in epithelioma papulosum cyprini cells

Environmental endocrine disrupting chemical 4-tert-butylphenol induced calcium overload and subsequent autophagy impairment via miRNA-363/CACNA1D Axis in epithelioma papulosum cyprini cells

Dexmedetomidine ameliorates acute kidney injury by regulating mitochondrial dynamics via the α2-AR/SIRT1/PGC-1α pathway activation in rats

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