Ubiquitin-specific protease 7 promotes ferroptosis via activation of the p53/TfR1 pathway in the rat hearts after ischemia/reperfusion

Tang, Lanhua; Zhou, Yuan-Jing; Xiong, Xiaofang; Li, Nian-Sheng; Zhang, Jie-Jie; Luo, Xiu-Ju; Peng, Jun

doi:10.1016/j.freeradbiomed.2020.10.307

Cited by 180 publications

(104 citation statements)

References 27 publications

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“…Ni et al found that targeting HIF-1α can induce osteoclast ferroptosis to treat osteoporosis (30). Some studies have shown that p53 can be used to regulate ferroptosis and mediate certain diseases (31,32). The above studies have proved the regulatory relationship between signaling pathways and ferroptosis in different disease types, which also con rms the trustworthiness of the signatures we have constructed from the side.…”

Section: Discussionsupporting

confidence: 57%

Ferroptosis-Related Long Non-Coding RNAs and the Roles of LASTR in Stomach Adenocarcinoma

Wang¹,

Sun²,

Wang³

et al. 2021

Preprint

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Background: Ferroptosis is a form of cell death involved in diverse physiological context. Increasing evidence suggests that there is a closely regulatory relationship between ferroptosis and long noncoding RNAs (lncRNAs).Method: RNA-sequencing data from The Cancer Genome Atlas (TCGA) data resource and ferroptosis-related genes from FerrDb (http://www.zhounan.org/ferrdb/) data resource were employed to select differentially expressed lncRNAs. We performed Univariate Cox regression and multivariate Cox analyses analysis on these differentially expressed lncRNAs to screen independent predictive factors. Subsequently, we established two signatures for predicting overall survival (OS) and progression-free survival (PFS). Finally, experiments were conducted to verify the roles of LASTR in gastric cancer (GC).Results: We identified 12 differentially expressed lncRNAs linked with OS and 13 associated with PFS. Kaplan-Meier(K-M) analyses exhibited that the high-risk group was related to a poor prognosis of stomach adenocarcinoma (STAD). The AUCs of the OS, as well as PFS signatures of lncRNAs were 0.734 and 0.771, respectively, indicating their excellent efficacy in predicting STAD prognosis. Our experimental results illustrated that the inhibition of LASTR inhibited tumor proliferation and migration in GC.Conclusion: This comprehensive evaluation of the ferroptosis-related lncRNA landscape in STAD unearthed novel lncRNAs related to carcinogenesis. In addition, we also experimentally confirmed the effects of LASTR on proliferation, migration and ferroptosis. These results provide potential novel targets for tumor treatment and promote personalized medicine.

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Section: Discussionsupporting

confidence: 57%

Ferroptosis-Related Long Non-Coding RNAs and the Roles of LASTR in Stomach Adenocarcinoma

Wang¹,

Sun²,

Wang³

et al. 2021

Preprint

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“…Transferrin receptor 1 (TfR1) is involved in cellular iron uptake. A novel pathway of ubiquitin-specific protease 7 (USP7)/p53/TfR1 is found in rat hearts after I/R treatment, and the upregulation of USP7 accelerates ferroptosis by activating the p53/TfR1 pathway [ 74 ]. The study has shown that ferroptosis occurs during reperfusion in rat hearts subjected to I/R [ 52 ].…”

Section: Pathological Mechanisms and Potential Targeted Therapy Of Ferroptosis In Ischemia-reperfusion Injurymentioning

confidence: 99%

Targeting Ferroptosis: Pathological Mechanism and Treatment of Ischemia‐Reperfusion Injury

et al. 2021

Oxidative Medicine and Cellular Longevity

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Ischemia-reperfusion (I/R) is a pathological process that occurs in many organs and diseases. Reperfusion, recovery of blood flow, and reoxygenation often lead to reperfusion injury. Drug therapy and early reperfusion therapy can reduce tissue injury and cell necrosis caused by ischemia, leading to irreversible I/R injury. Ferroptosis was clearly defined in 2012 as a newly discovered iron-dependent, peroxide-driven, nonapoptotic form of regulated cell death. Ferroptosis is considered the cause of reperfusion injury. This discovery provides new avenues for the recognition and treatment of diseases. Ferroptosis is a key factor that leads to I/R injury and organ failure. Given the important role of ferroptosis in I/R injury, there is considerable interest in the potential role of ferroptosis as a targeted treatment for a wide range of I/R injury-related diseases. Recently, substantial progress has been made in applying ferroptosis to I/R injury in various organs and diseases. The development of ferroptosis regulators is expected to provide new opportunities for the treatment of I/R injury. Herein, we analytically review the pathological mechanism and targeted treatment of ferroptosis in I/R and related diseases from the perspectives of myocardial I/R injury, cerebral I/R injury, and ischemic renal injury.

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“… Ma et al (2020) demonstrated that USP22 (ubiquitin-specific protease 22), a member of the deubiquitinase family, could inhibit ferroptosis in myocardial IRI via the SIRT1/p53/SLC7A11 association. On the contrary, USP7 is found to protect cardiomyocytes against ferroptosis caused by IRI via activation of the p53/TfR1 pathway ( Tang et al, 2021b ). Likewise, ferroptosis is demonstrated to be associated with diabetes myocardial IRI.…”

Section: Ferroptosis and Cvdsmentioning

confidence: 99%

Targeting Ferroptosis to Treat Cardiovascular Diseases: A New Continent to Be Explored

Huang

Yang

Xiao

et al. 2021

Front. Cell Dev. Biol.

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Cardiovascular diseases, including cardiomyopathy, myocardial infarction, myocardial ischemia/reperfusion injury, heart failure, vascular injury, stroke, and arrhythmia, are correlated with cardiac and vascular cell death. Ferroptosis is a novel form of non-apoptotic regulated cell death which is characterized by an iron-driven accumulation of lethal lipid hydroperoxides. The initiation and execution of ferroptosis are under the control of several mechanisms, including iron metabolism, glutamine metabolism, and lipid peroxidation. Recently, emerging evidence has demonstrated that ferroptosis can play an essential role in the development of various cardiovascular diseases. Recent researches have shown the ferroptosis inhibitors, iron chelators, genetic manipulations, and antioxidants can alleviate myocardial injury by blocking ferroptosis pathway. In this review, we systematically described the mechanisms of ferroptosis and discussed the role of ferroptosis as a novel therapeutic strategy in the treatment of cardiovascular diseases.

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Ubiquitin-specific protease 7 promotes ferroptosis via activation of the p53/TfR1 pathway in the rat hearts after ischemia/reperfusion

Cited by 180 publications

References 27 publications

Ferroptosis-Related Long Non-Coding RNAs and the Roles of LASTR in Stomach Adenocarcinoma

Ferroptosis-Related Long Non-Coding RNAs and the Roles of LASTR in Stomach Adenocarcinoma

Targeting Ferroptosis: Pathological Mechanism and Treatment of Ischemia‐Reperfusion Injury

Targeting Ferroptosis to Treat Cardiovascular Diseases: A New Continent to Be Explored

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