Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

Xu, Hongen; Zhang, Juqi; Gong, Mingli; Gu, Yanlun; Dong, Bingqi; Pang, Xu; Zhang, Chenglong; Chen, Yimin

doi:10.3389/fimmu.2023.1197275

Cited by 7 publications

(1 citation statement)

References 41 publications

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“…The pathogenesis of RA has been shown to be associated with the hub genes PTGS2 , ENO1 , and GRN , which are strongly associated with ferroptosis. [ 20 ] The abnormal proliferation of synovial fibroblasts in RA may be attributed to reduced ferroptosis sensitivity in FLSs. One mechanism involves S-adenosylmethionine (SAM), which decreases the expression of GPX4 and ferritin heavy polypeptide 1 (FTH1) in RA-FLSs by promoting and mediating GPX4 promoter methylation and reducing FTH1 expression.…”

Section: Iron Metabolism and Arthritismentioning

confidence: 99%

Iron metabolism and arthritis: Exploring connections and therapeutic avenues

Zhuo,

Xiao,

Tang

et al. 2024

Chinese Medical Journal

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Iron is indispensable for the viablility of nearly all living organisms, and it is imperative for cells, tissues, and organisms to acquire this essential metal sufficiently and maintain its metabolic stability for survival. Disruption of iron homeostasis can lead to the development of various diseases. There is a robust connection between iron metabolism and infection, immunity, inflammation, and aging, suggesting that disorders in iron metabolism may contribute to the pathogenesis of arthritis. Numerous studies have focused on the significant role of iron metabolism in the development of arthritis and its potential for targeted drug therapy. Targeting iron metabolism offers a promising approach for individualized treatment of arthritis. Therefore, this review aimed to investigate the mechanisms by which the body maintains iron metabolism and the impacts of iron and iron metabolism disorders on arthritis. Furthermore, this review aimed to identify potential therapeutic targets and active substances related to iron metabolism, which could provide promising research directions in this field.

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Section: Iron Metabolism and Arthritismentioning

confidence: 99%

Iron metabolism and arthritis: Exploring connections and therapeutic avenues

Zhuo,

Xiao,

Tang

et al. 2024

Chinese Medical Journal

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Ferroptosis defense mechanisms: The future and hope for treating osteosarcoma

Ma,

Cong,

Shen

et al. 2024

Cell Biochemistry & Function

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Currently, challenges such as chemotherapy resistance, resulting from preoperative and postoperative chemotherapy, postoperative recurrence, and poor bone regeneration quality, are becoming increasingly prominent in osteosarcoma (OS) treatment. There is an urgent need to find more effective ways to address these issues. Ferroptosis is a novel form of iron‐dependent programmed cell death, distinct from other forms of cell death. In this paper, we summarize how, through the three major defense systems of ferroptosis, not only can substances from traditional Chinese medicine, antitumor drugs, and nano‐drug carriers induce ferroptosis in OS cells, but they can also be combined with immunotherapy, differentiation therapy, and other treatment modalities to significantly enhance chemotherapy sensitivity and inhibit tumor growth. Thus, ferroptosis holds great potential in treating OS, offering more choices and possibilities for future clinical interventions.

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Knockdown of ENO1 promotes autophagy dependent‐ferroptosis and suppresses glycolysis in breast cancer cells via the regulation of CST1

Huang,

Lu,

You

et al. 2024

Drug Development Research

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Autophagy‐dependent ferroptosis and glycolysis play a significant role in tumor development. α‐Enolase (ENO1), a glycolytic enzyme, has been demonstrated to function as a crucial modulator in breast cancer (BC). However, the specific mechanism by which ENO1 influences the ferroptosis and glycolysis of BC remains unclear. qRT‐PCR, along with western blot analysis was applied to investigate ENO1 and cystatin SN (CST1) expression in BC cells. Glycolysis level was measured by extracellular acidification rate (ECAR), lactate production, glucose consumption, and western blot analysis. Ferroptosis was evaluated by iron and lipid peroxidation assay, DCFH‐DA staining, and western blot analysis. Immunofluorescence, together with western blot analysis was adopted for assessing cell autophagy and mTOR signaling pathway. Cell apoptosis and Ki67 level were measured by TUNEL and immunohistochemistry, respectively. ENO1 had abundant existence in BC cell lines. ENO1 silencing inhibited glycolysis but promoted ferroptosis and autophagy. In addition, autophagy inhibitor 3‐MA reversed the impacts of ENO1 silencing on glycolysis and ferroptosis. Meanwhile, mTOR activator MHY1485 demonstrated opposing effects on autophagy. Moreover, CST1 could be extensively found in BC cell lines, and its overexpression reversed the effects of ENO1 silencing on glycolysis and ferroptosis. In vivo experiments illustrated that ENO1 deletion suppressed BC tumor growth, increased the apoptosis rate, restrained cell proliferation, and glycolysis, but promoted ferroptosis and autophagy, as well as reducing CST1 and mTOR signaling. To sum up, ENO1 silencing mediated a utophagy‐dependent ferroptosis and glycolysis in BC cells by regulating CST1.

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Identification of potential ferroptosis-associated biomarkers in rheumatoid arthritis

Cited by 7 publications

References 41 publications

Iron metabolism and arthritis: Exploring connections and therapeutic avenues

Iron metabolism and arthritis: Exploring connections and therapeutic avenues

Ferroptosis defense mechanisms: The future and hope for treating osteosarcoma

Knockdown of ENO1 promotes autophagy dependent‐ferroptosis and suppresses glycolysis in breast cancer cells via the regulation of CST1

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