PSTPIP2 inhibits cisplatin-induced acute kidney injury by suppressing apoptosis of renal tubular epithelial cells

Zhu, Hong; Jiang, Wenjuan; Zhao, Huizi; He, Changsheng; Tang, Xiao‐Han; Xu, Songbing; Chen, Xu; Feng, Rui; Li, Jun; Ma, Tran; Huang, Cheng

doi:10.1038/s41419-020-03267-2

Cited by 34 publications

(22 citation statements)

References 36 publications

(40 reference statements)

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“…In AKI induced by I/R, a metabolic reprogramming also has been reported with a glycolytic shift and PDC inhibition [ 29 ], indicating a decreased activity of this enzyme complex and ergo a reduction in acetyl-CoA synthesis; moreover, in AKI induced by cisplatin, H3K27 acetylation is reduced, and the restoration of its acetylation levels decreases kidney damage [ 30 , 31 ]. Hence, in CKD and AKI, there appears to be a decrease in acetyl-CoA levels, which in turn impacts histone acetylation.…”

Section: Acetyl-coamentioning

confidence: 99%

Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases

et al. 2021

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Mitochondria are complex organelles that orchestrate several functions in the cell. The primary function recognized is energy production; however, other functions involve the communication with the rest of the cell through reactive oxygen species (ROS), calcium influx, mitochondrial DNA (mtDNA), adenosine triphosphate (ATP) levels, cytochrome c release, and also through tricarboxylic acid (TCA) metabolites. Kidney function highly depends on mitochondria; hence mitochondrial dysfunction is associated with kidney diseases. In addition to oxidative phosphorylation impairment, other mitochondrial abnormalities have been described in kidney diseases, such as induction of mitophagy, intrinsic pathway of apoptosis, and releasing molecules to communicate to the rest of the cell. The TCA cycle is a metabolic pathway whose primary function is to generate electrons to feed the electron transport system (ETS) to drives energy production. However, TCA cycle metabolites can also release from mitochondria or produced in the cytosol to exert different functions and modify cell behavior. Here we review the involvement of some of the functions of TCA metabolites in kidney diseases.

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Section: Acetyl-coamentioning

confidence: 99%

Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases

et al. 2021

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“…Cisplatin-induced nephrotoxicity is accompanied by apoptosis of renal tubular epithelial cells, and suppression of renal tubular epithelial cell apoptosis reduces nephrotoxicity [12]. A previous study showed that ruscogenin represses lipopolysaccharide-induced apoptosis of pulmonary endothelial cells [8].…”

Section: Discussionmentioning

confidence: 98%

Ruscogenin protects against cisplatin-induced apoptosis, inflammation, and oxidative stress of renal tubular epithelial cells

Yu¹,

Feng²,

Li³

et al. 2022

Trop. J. Pharm Res

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Purpose: To determine the potential effect of ruscogenin in cisplatin-induced nephrotoxicity. Methods: Rat renal tubular epithelial cells (NRK-52E) were treated with 50 μM cisplatin to establish an in vitro cell model of nephrotoxicity. Cytotoxicity was assessed by MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay, flow cytometry, and western blot. Different concentrations of ruscogenin (2.5, 5, and 10 μM) were incubated with cisplatin-treated NRK-52E cells. Alterations in the nod-like receptor family, the pyrin domain-containing protein (NLRP3) inflammasome, toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB), and nuclear factor erythropoietin-2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) components were determined using western blot. Flow cytometry was also used to investigate the levels of reactive oxygen species (ROS). Results: Ruscogenin significantly increased cell viability (p < 0.01) and suppressed apoptosis of NRK- 52E cells (p < 0.01), attenuating cisplatin-induced cytotoxicity. The NLRP3 inflammasome was activated in cisplatin-treated NRK-52E cells with enhanced NLRP3, interleukin 1 beta, and cleaved caspase-1; however, ruscogenin significantly decreased the expression of NLRP3 inflammasome components (p < 0.01). Ruscogenin attenuated cisplatin-induced expression of TLR4, myeloid differentiation primary response 88, and NF-κB. Further, cisplatin induction enhanced ROS formation, with increased malondialdehyde and decreased glutathione reductase and catalase levels. Ruscogenin attenuated cisplatin-induced ROS accumulation in NRK-52E cells through up-regulation of Nrf2 and HO-1. Conclusion: Ruscogenin protects against cisplatin-induced apoptosis, inflammation, and oxidative stress in renal tubular epithelial cells via suppression of TLR4/NF-κB activation and promotion of Nrf2/HO-1 activation. Therefore, ruscogenin provides a potential therapeutic strategy for mitigating cisplatin-induced nephrotoxicity.

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“…Induction of Nrf2 signalling pathway was also observed in common carp (Kövesi et al 2020b ). The experiment conducted on human hepatocytes L02 cells revealed that caveolin-1 (CAV-1) interacts with Nrf2 in response to oxidative stress caused by AFB1 to trigger apoptosis in cells (Xu et al 2020 ). A decrease in Nrf2 and HO-1 expression was also noticed in Wistar rats exposed to AFB1 and interestingly that effect was partially restored by administration of antidiabetic drug Sitagliptin (Ji et al 2020 ).…”

Section: Mycotoxinsmentioning

confidence: 99%

Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

Kozieł

Kowalska

Piastowska-Ciesielska

2021

Arch Toxicol

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Nuclear factor erythroid 2-like 2 (Nrf2) is a transcription factor participating in response to cellular oxidative stress to maintain the redox balance. Generation of reactive oxygen species (ROS) and, in consequence, oxidative stress, are physiological as well as pathological processes which take place in almost all types of cells. Nrf2, in response to oxidative stress, activates expression and production of antioxidant enzymes to remove free radicals. However, the role of Nrf2 seems to be more sophisticated and its increased expression observed in cancer cells allows to draw a conclusion that its role is tissue—and condition—dependent. Interestingly, Nrf2 might also play a crucial role in response to environmental factors like mycotoxins. Thus, the aim of the study is to review the role of Nrf2 in cells exposed to most common mycotoxins to check if the Nrf2 signaling pathway serves as the main response element to mycotoxin-induced oxidative stress in human and animal cells and if it can be a target of detoxifying agents.

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PSTPIP2 inhibits cisplatin-induced acute kidney injury by suppressing apoptosis of renal tubular epithelial cells

Cited by 34 publications

References 36 publications

Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases

Involvement of Tricarboxylic Acid Cycle Metabolites in Kidney Diseases

Ruscogenin protects against cisplatin-induced apoptosis, inflammation, and oxidative stress of renal tubular epithelial cells

Nrf2: a main responsive element in cells to mycotoxin-induced toxicity

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