Fisetin treatment alleviates kidney injury in mice with diabetes-exacerbated atherosclerosis through inhibiting CD36/fibrosis pathway

Zou, Ting-feng; Liu, Zhigang; Cao, Peichang; Zheng, Shihong; Guo, Weiwen; Wang, Tianxiang; Chen, Yuan-li; Duan, Yajun; Liu, Qingshan; Liao, Chen-zhong; Xie, Zhouling; Han, Jihong; Yang, Xiaoxiao

doi:10.1038/s41401-023-01106-6

Cited by 9 publications

(2 citation statements)

References 49 publications

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“…For example, the modulation of MMP9 expression was predominantly achieved through the inhibition of signaling pathways involving transforming growth factor‐β and SMAD family members 2/3 (Smad2/3). 53 The PLOD2 enzymes play a pivotal role in the posttranslational modification and folding of collagen, culminating in the formation of an inflexible ECM that triggers the expression of genes associated with EMT and cancer stem cells, leading to metastatic dissemination of cancer. 54 The IL‐7R receptor licenses a population of memory CD8 + T cells that exhibit superior efficacy in antitumor responses.…”

Section: Discussionmentioning

confidence: 99%

Enhancing the revelation of key genes and interaction networks in non‐small cell lung cancer with major depressive disorder: A bioinformatics analysis

Gui,

Chen,

Nie

et al. 2024

Health Science Reports

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Background and AimsLung cancer is ranked as the second most prevalent form of cancer worldwide. Nonsmall cell lung cancer (NSCLC) represents the predominant histological subtype. Research suggests that one‐third of lung cancer patients also experiencing depression. Antidepressants play an indispensable role in the management of NSCLC. Despite significant advancements in treatment, lung cancer patients still face a high mortality rate. Major depressive disorder (MDD) and related antidepressants involved in treatment efficacy and prognosis of NSCLC. However, there has been a lack of screening and analysis regarding genes and networks associated with both NSCLC and MDD.MethodsTo investigate the correlation between MDD and NSCLC, our discovery and validation analysis included four datasets from the Gene Expression Omnibus database from NSCLC or MDD. Differential gene expression (DEGs) analysis, GO and KEGG Pathway, and protein‐protein interaction network analyzes to identify hub genes, networks, and associated observations link between MDD and NSCLC.ResultsThe analysis of two datasets yielded a total of 84 downregulated and 52 upregulated DEGs. Pathway enrichment analyzes indicated that co‐upregulated genes were enriched in the regulation of positive regulation of cellular development, collagen‐containing extracellular matrix (ECM), cytokine binding, and axon guidance. We identified 20 key genes, which were further analyzed using the MCODE plugin to identify two core subnetworks. The integration of functionally similar genes provided valuable insights into the potential involvement of these hub genes in diverse biological processes including angiogenesis humoral immune response regulation inflammatory response organization ECM network.ConclusionWe have identified a total of 136 DEGs that participate in multiple biological signaling pathways. A total of 20 hub genes have demonstrated robust associations, potentially indicating novel diagnostic and therapeutic targets for both diseases.

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Section: Discussionmentioning

confidence: 99%

Enhancing the revelation of key genes and interaction networks in non‐small cell lung cancer with major depressive disorder: A bioinformatics analysis

Gui,

Chen,

Nie

et al. 2024

Health Science Reports

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“…The mice of the control group and ApoE −/− group were given an oral gavage with 0.2 mL water every day. The mice in the fisetin-treated ApoE −/− group were administered fisetin at a dose of 20 mg/kg every day according to previous studies [17][18][19]. All mice were treated every day for 12 weeks.…”

Section: Animals and Treatmentmentioning

confidence: 99%

Fisetin Suppresses Atherosclerosis by Inhibiting Ferroptosis-Related Oxidative Stress in Apolipoprotein E Knockout Mice

Jiang,

Lei,

Yin

et al. 2024

Pharmacology

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Introduction: Fisetin has been demonstrated to inhibit the occurrence of atherosclerosis, however, the mechanism of fisetin suppressing atherosclerosis remains elusive. Methods: The function of fisetin in the inhibition of atherosclerosis was evaluated by hematoxylin and eosin and Oil Red O staining in ApoE-/- mice. Molecular biomarkers of atherosclerosis progression were detected by Western blot and qPCR. Moreover, the inhibition of atherosclerosis on oxidative stress and ferroptosis was evaluated by immunofluorescence staining, qPCR and Western blot assays. Results: The obtained results showed that serum lipid was attenuated and consequentially the formation of atherosclerosis was also suppressed by fisetin in ApoE-/- mice. Exploration of the mechanism revealed that molecular biomarkers of atherosclerosis were decreased under fisetin treatment. The level of reactive oxygen species and malondialdehyde declined, while the activity of superoxide dismutases and glutathione peroxidase was increased under the fisetin treatment. Additionally, the suppressor of ferroptosis, glutathione peroxidase 4 protein, was elevated. The ferritin was decreased in the aortic tissues treated with fisetin. Conclusions: In summary, fisetin attenuated the formation of atherosclerosis through the inhibition of oxidative stress and ferroptosis in the aortic tissues of ApoE-/- mice.

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Curcumin Interferes with TGF- β 1-Induced Fibrosis in NRK-49F Cells by Reversing ADAMTS18 Gene Methylation

Xu,

Zhang,

et al. 2023

Chin. J. Integr. Med.

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Fisetin treatment alleviates kidney injury in mice with diabetes-exacerbated atherosclerosis through inhibiting CD36/fibrosis pathway

Cited by 9 publications

References 49 publications

Enhancing the revelation of key genes and interaction networks in non‐small cell lung cancer with major depressive disorder: A bioinformatics analysis

Enhancing the revelation of key genes and interaction networks in non‐small cell lung cancer with major depressive disorder: A bioinformatics analysis

Fisetin Suppresses Atherosclerosis by Inhibiting Ferroptosis-Related Oxidative Stress in Apolipoprotein E Knockout Mice

Curcumin Interferes with TGF- β 1-Induced Fibrosis in NRK-49F Cells by Reversing ADAMTS18 Gene Methylation

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