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Keywords {🔍}

pubmed, google, scholar, cas, zhang, han, yang, wang, mercury, mitochondrial, liu, pathway, environ, central, article, exposure, kidney, cell, sci, cells, stress, induced, methodology, inorganic, dynamics, oxidative, analysis, effects, signaling, jiang, apoptosis, conceptualization, data, information, disorder, deng, human, hgcl, induces, privacy, cookies, content, research, renal, injury, hek, access, mercuric, chloride, author,

Topics {✒️}

sirt1/nrf2/tnf-alpha signaling pathway sirt1/pgc-1 alpha/nrf2 pathway akt/gsk-3 beta/fyn pathway cytokine-mediated cell-cell interactions inflammasome/nf-κb translocation inhibition sesn2/ampk/nrf2 signaling pathway sirt1/pgc-1 alpha pathway estrogen-related receptor-alpha sirt1/pgc-1α adenosine-triphosphate qrt-pcr imidacloprid-induced liver fibrosis month download article/chapter tgf-beta 1/smad pathway cgas-sting signaling pathway nrf2/tslp/jak1 pathway chronic arsenic exposure isolated rat hepatocytes renal injury induced induced cardiac injury mitochondrial dynamics disorder project administration writing–review mercuric chloride poisoning nrf2-antioxidant pathway activation hepatotoxicity induced liver fibrosis induced ampk/nrf2 pathway animal disease control pgc-1α mitochondrial dynamics/mitophagy hgcl2 induces hek-293 related subjects fibrogenic response induced full article pdf hgcl2 exposure resulted sesn2-mediated impairment privacy choices/manage cookies inorganic mercury exposure pgc-1 alpha mercury chloride toxicity upregulation mitochondrial fission mercuric chloride human health impacts inorganic mercury accumulates excessive oxidative stress amino acid carriers excess fatty acid dietary luteolin protects compensatory renal growth sh-sy5y cells hexavalent chromium

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         headline:Harmful Effects of Inorganic Mercury Exposure on Kidney Cells: Mitochondrial Dynamics Disorder and Excessive Oxidative Stress
         description:Mercury is widely used in industry and has caused global environmental pollution. Inorganic mercury accumulates in the body causes damage to many organs, and the kidney is the most susceptible to the toxic effects of mercury. However, the underlying specific molecular mechanism of renal injury induced by inorganic mercury remains unclear at the cellular level. Therefore, in order to understand its molecular mechanism, we used in vitro method. We established experimental models by treating human embryonic kidney epithelial cell line (HEK-293 T) cells with HgCl2 (0, 1.25, 5, and 20 µmol/L). We found that HgCl2 can lead to a decrease in cell viability and oxidative stress of HEK-293 T, which may be mediated by upregulation mitochondrial fission. In addition, HgCl2 exposure resulted in the mitochondrial disorder of HEK-293 T cells, which was mediated by downregulating the expression of silent information regulator two ortholog 1 (Sirt1)/peroxisome proliferator–activated receptor coactivator-1α (PGC-1α) signaling pathway. In summary, our results suggest that HgCl2 induces HEK-293 T cell toxicity through promoting Sirt1/PGC-1α axis-mediated mitochondrial dynamics disorder and oxidative stress. Sirt1/PGC-1α may be an appealing pharmaceutical target curing HgCl2-induced kidney injury.
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      headline:Harmful Effects of Inorganic Mercury Exposure on Kidney Cells: Mitochondrial Dynamics Disorder and Excessive Oxidative Stress
      description:Mercury is widely used in industry and has caused global environmental pollution. Inorganic mercury accumulates in the body causes damage to many organs, and the kidney is the most susceptible to the toxic effects of mercury. However, the underlying specific molecular mechanism of renal injury induced by inorganic mercury remains unclear at the cellular level. Therefore, in order to understand its molecular mechanism, we used in vitro method. We established experimental models by treating human embryonic kidney epithelial cell line (HEK-293 T) cells with HgCl2 (0, 1.25, 5, and 20 µmol/L). We found that HgCl2 can lead to a decrease in cell viability and oxidative stress of HEK-293 T, which may be mediated by upregulation mitochondrial fission. In addition, HgCl2 exposure resulted in the mitochondrial disorder of HEK-293 T cells, which was mediated by downregulating the expression of silent information regulator two ortholog 1 (Sirt1)/peroxisome proliferator–activated receptor coactivator-1α (PGC-1α) signaling pathway. In summary, our results suggest that HgCl2 induces HEK-293 T cell toxicity through promoting Sirt1/PGC-1α axis-mediated mitochondrial dynamics disorder and oxidative stress. Sirt1/PGC-1α may be an appealing pharmaceutical target curing HgCl2-induced kidney injury.
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