Targeting ferroptosis in acute kidney injury

Ni, Lihua; Yuan, Cheng; Wu, Xiaoyan

doi:10.1038/s41419-022-04628-9

Cited by 92 publications

(56 citation statements)

References 177 publications

(141 reference statements)

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“…In past studies on iron toxicity, features of iron toxicity were found to include accumulation of lipid peroxides, disturbances in iron metabolism, accumulation of ROS and the consumption of GPX4 and system Xc- (a cysteine/glutamate antiporter system). ( Ni et al, 2022 ). Biochemically, ferroptosis mainly includes the consumption of glutathione (GSH) and the decreased activity of GPX4 ( Zheng and Conrad, 2020 ; Obeng, 2021 ).…”

Section: Resultsmentioning

confidence: 99%

Preparation, structural characterization, antioxidant activity and protection against cisplatin-induced acute kidney injury by polysaccharides from the lateral root of Aconitum carmichaelii

et al. 2022

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Response surface methodology (RSM) and Box- Behnken design (BBD) based on one-way experiments were used to optimize the extraction parameters of the lateral root polysaccharides of Aconitum carmichaelii. The extracted polysaccharides were named as refined fucose polysaccharide. The optimal conditions included a water to raw material ratio of 43, an extraction time of 2 h, and an extraction temperature of 90°C. The shape of RFP was shown by infrared spectroscopy (IR) and scanning electron microscopy (SEM) analysis. The monosaccharide composition and molecular weight of RFP was determined by high-performance liquid chromatography (HPLC). Furthermore, RFP exhibited moderate antioxidant activity by analyzing the scavenging rates of 2,2-diphenyl-1-picrylhydrazyl radical, superoxide anion radical, hydroxyl radical, and ABTS + radical. RFP exerted cytoprotective effects against hydrogen peroxide (H2O2)-induced injury in the rat renal tubular epithelial cell line rat renal tubular epithelial cells (NRK-52E) and inhibited apoptosis. In addition, researches found that RFP could alleviate cisplatin-induced acute kidney injury in mice by enhancing the levels of glutathione (GSH) and glutathione peroxidase-4 (GPX-4), decreasing the levels of malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), reducing lipid peroxidation, and thus inhibiting ferroptosis. In conclusion, this study provides a good strategy for obtaining bioactive polysaccharides from Fuzi.

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Section: Resultsmentioning

confidence: 99%

Preparation, structural characterization, antioxidant activity and protection against cisplatin-induced acute kidney injury by polysaccharides from the lateral root of Aconitum carmichaelii

et al. 2022

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“…TECs undergo various types of programmed cell death (PCD) including apoptosis, pyroptosis, necroptosis, and ferroptosis (64)(65)(66)(67). Upon sensing local tissue injury, resident and infiltrating inflammatory cells in the kidney promote TEC PCD by producing and releasing large amounts of inflammatory cytokines and activating various pathway proteins, leading to TEC detachment, tubular occlusion, and tubular inactivation.…”

Section: Immune Cells Promote Various Types Of Programmed Cell Deaths...mentioning

confidence: 99%

Interaction Between Intrinsic Renal Cells and Immune Cells in the Progression of Acute Kidney Injury

Deng

et al. 2022

Front. Med.

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A growing number of studies have confirmed that immune cells play various key roles in the pathophysiology of acute kidney injury (AKI) development. After the resident immune cells and intrinsic renal cells are damaged by ischemia and hypoxia, drugs and toxins, more immune cells will be recruited to infiltrate through the release of chemokines, while the intrinsic cells promote macrophage polarity conversion, and the immune cells will promote various programmed deaths, phenotypic conversion and cycle arrest of the intrinsic cells, ultimately leading to renal impairment and fibrosis. In the complex and dynamic immune microenvironment of AKI, the bidirectional interaction between immune cells and intrinsic renal cells affects the prognosis of the kidney and the progression of fibrosis, and determines the ultimate fate of the kidney.

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“…Several novel therapeutic agents that inhibit necroptosis have already shown efficacy in experimental studies, and human translation appears to be promising [13 && ]. Ferroptosis, a distinct form of nonapoptotic irondependent cell death now well described in AKI, is characterized primarily by intracellular accumulation of labile, catalytic iron, with subsequent lipid peroxidation, membrane rupture and cell death [12,15,16]. Targeted inhibition of ferroptosis via widely available lipophilic antioxidants and iron chelators are achieving promising preliminary results.…”

Section: Alterations In Tubule Cell Deathmentioning

confidence: 99%

Pathogenesis of intrinsic acute kidney injury

Devarajan

2022

Current Opinion in Pediatrics

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Purpose of reviewThis review focuses on the pathogenesis of intrinsic acute kidney injury (AKI), emphasizing recent advances that hold therapeutic promise.Recent findingsEnhanced endothelin and reduced endothelium-derived nitric oxide release in AKI can be blocked using endothelin receptor antagonists or nitric oxide supplementation. Vasodilatory agents such as theophylline and caffeine may prevent AKI. Free labile iron is a potent factor in the generation of reactive oxygen species and tubule damage in AKI. Apoptosis via induction of p53 is an important mechanism of cell death in AKI, which can be blocked using small interfering RNA. The AKI-driven reduction in nicotinamide adenine dinucleotide can be countered using oral supplements. Surviving tubule cells regenerate after AKI, by upregulating genes encoding growth factors, such as hepatocyte growth factor. Pro-angiogenic agents (statins and erythropoietin) that can mobilize endothelial progenitor cells after AKI are currently being tested. The inflammatory response in AKI, including activation of C5a, can be therapeutically targeted. Contemporary single cell profiling technologies have identified novel genes with altered expression, new signalling pathways and drug targets in AKI.SummaryRecent advances in the pathogenesis of intrinsic AKI have provided a better understanding of the clinical continuum and the rational deployment of promising therapeutics.

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Targeting ferroptosis in acute kidney injury

Cited by 92 publications

References 177 publications

Preparation, structural characterization, antioxidant activity and protection against cisplatin-induced acute kidney injury by polysaccharides from the lateral root of Aconitum carmichaelii

Preparation, structural characterization, antioxidant activity and protection against cisplatin-induced acute kidney injury by polysaccharides from the lateral root of Aconitum carmichaelii

Interaction Between Intrinsic Renal Cells and Immune Cells in the Progression of Acute Kidney Injury

Pathogenesis of intrinsic acute kidney injury

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