CIRBP promotes ferroptosis by interacting with ELAVL1 and activating ferritinophagy during renal ischaemia‐reperfusion injury

Sui, Mingxing; Xu, Da; Zhao, Wen‐Yu; Lu, Heng; Chen, Rui; Duan, Yazhe; Li, Yanhua; Zhu, Youhua; Zhang, Lei; Zeng, Li

doi:10.1111/jcmm.16567

Cited by 37 publications

(32 citation statements)

References 39 publications

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“…Previous studies have suggested that targeting ferroptosis could prevent tubular injury, regulate the integrity of mitochondria, and alleviate inflammation via immune cells in rodent models of diabetic nephrology or AKI (Fig. 4 ) [ 118 – 121 ]. However, direct evidence about ferroptosis in the progression of AKI to CKD is lacking, which might be a hot point of research in the future.…”

Section: Ferroptosis In the Aki To Chronic Kidney Disease (Ckd) Progr...mentioning

confidence: 99%

Targeting ferroptosis in acute kidney injury

Yuan

2022

Cell Death Dis

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Acute kidney injury (AKI) is a major public health problem with high incidence and mortality. As a form of programmed cell death (PCD), ferroptosis could be considered as a process of iron accumulation and enhanced lipid peroxidation. Recently, the fundamental roles of ferroptosis in AKI have attracted much attention. The network mechanism of ferroptosis in AKI and its roles in the AKI to chronic kidney disease (CKD) transition is complicated and multifactorial. Strategies targeting ferroptosis show great potential. Here, we review the research progress on ferroptosis and its participation in AKI. We hope that this work will provide clues for further studies of ferroptosis in AKI.

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Section: Ferroptosis In the Aki To Chronic Kidney Disease (Ckd) Progr...mentioning

confidence: 99%

Targeting ferroptosis in acute kidney injury

Yuan

2022

Cell Death Dis

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“…Although there is a biochemical link between NCOA4-mediated ferritinophagy and ferroptosis, current findings have shown a positive correlation among them (i.e., NCOA4- mediated ferritinophagy can induce ferroptosis) [ 65 – 67 ]; therefore, the relationship between remains controversial. For example, NCOA4 levels varied by ferroptosis inducer, with increased expression reported in hepatic stellate cells (HSCs) after sorafenib treatment, no differential expression in pancreatic cancer cells after elastin treatment, and elastin therapy resulted in even lower levels in MEFs or artesunate treatment in HSCs [ 62 ].…”

Section: Ferroptosis Relation With Other Rcdsmentioning

confidence: 99%

Ferroptosis: A Novel Therapeutic Direction of Spinal Cord Injury

Zhao

Liu

Zhou

et al. 2022

Computational and Mathematical Methods in Medicine

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An injury to the spinal cord results in a crucial central nervous system event that further causes irreversible impairment or loss of motor, autonomic, and sensory functions. A progressive pathophysiological cascade following spinal cord injury (SCI) includes ischemia/reperfusion injury, oxidative stress, proapoptotic signaling, peripheral inflammatory cell infiltration, and glutamate-mediated excitotoxicity, and regulated cell death. These complex pathological and physiological changes continue to cause cell injury over the long-term and severely limit the efficacy of clinical treatment strategies in restoring the injured nervous system. Ferroptosis is a nonapoptotic, iron-regulated kind of cell death that has recently been discovered. It is distinguished by iron overload-induced toxic lipid peroxidation associated with mitochondrial morphological changes during the cell death process. For example, after SCI, iron overload activates the reactive oxygen species generation, dysregulation of glutathione/glutathione peroxidase 4 (GSH/GPX4) metabolism, and accumulation of lipid peroxides, which cause lipid membrane deterioration and ferroptosis. Conversely, knockout or differential expression of key genes and application of lipid peroxidation inhibitors and iron chelators (e.g., deferoxamine) (e.g., SRS-16-86) can block ferroptosis and promote neuronal repair for functional recovery after SCI. Although the findings of numerous investigations have been confirmed the importance of ferroptosis in several human neurologic sicknesses and its potential in SCI, the mechanism of ferroptosis and its application in SCI has not been elucidated. This review highlights current ferroptosis research and its impact on SCI, as well as the key molecular mechanism of ferroptosis in promoting the recovery from SCI. Understanding ferroptosis’ process and function in SCI could provide useful insight into the treatment and avoidance of such a destructive injury.

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“…This further confirmed that cold induction could promote the process of ferroptosis by inducing the expression of CIRBP and then regulating key factors such as p53 and GPX4. Ferroptosis inducer erastin or hypoxia-reoxygenation (HR) treatment induced renal tubular epithelial cells to express CIRBP, and silencing of CIRBP inhibited ferroptosis induced by HR or erastin [ 20 ]. Therefore, CIRBP is also a key factor regulating the progression of ferroptosis.…”

Section: Discussionmentioning

confidence: 99%

CIRBP Regulates Pancreatic Cancer Cell Ferroptosis and Growth by Directly Binding to p53

Gao

Xie

Huang

et al. 2022

Journal of Immunology Research

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Pancreatic cancer is one of the most malignant gastrointestinal tumors, and it is of great significance to explore the molecular mechanism of its progression and find new biological therapeutic targets. CIRBP is a cold-induced protein that plays a key role in many physiological and pathological processes, but its role in pancreatic cancer is still unclear. The expression of CIRBP in pancreatic cancer tissues was slightly lower than that in normal tissues, and the high expression of CIRBP was beneficial to survival. At the same time, immunohistochemical detection showed that the expression level of CIRBP in the cytoplasm of cancer tissues was significantly lower than that of adjacent tissues; survival curve analysis showed that pancreatic cancer patients with high nuclear CIRBP expression had a longer overall survival period. RIP results showed that CIRBP antibody significantly enriched p53 RNA, indicating that it could directly bind to p53. Cold treatment of pancreatic cancer cells significantly induced the expression of CIRBP, DPP4, NOX1, and FTH1 and inhibited the expression of p53 and GPX4. Cold induction enhanced the accumulation of Fe2+ in cells, promoted the generation of ROS, and inhibited the expression of GSH-Px. Therefore, cold induction promotes the process of ferroptosis by inducing the expression of CIRBP and then regulating key factors such as p53 and GPX4. In addition, cold induction significantly inhibited the proliferation of pancreatic cancer cells and induced cell apoptosis, but after the addition of ferroptosis inhibitor, cell proliferation and apoptosis did not change significantly. Therefore, CIRBP acts as a tumor suppressor gene in pancreatic cancer and induces ferroptosis through the p53/GPX4 pathway to inhibit cell growth, which may be an important target for the diagnosis and treatment of pancreatic cancer.

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CIRBP promotes ferroptosis by interacting with ELAVL1 and activating ferritinophagy during renal ischaemia‐reperfusion injury

Cited by 37 publications

References 39 publications

Targeting ferroptosis in acute kidney injury

Targeting ferroptosis in acute kidney injury

Ferroptosis: A Novel Therapeutic Direction of Spinal Cord Injury

CIRBP Regulates Pancreatic Cancer Cell Ferroptosis and Growth by Directly Binding to p53

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