Targeting Ferroptosis in Bone-Related Diseases: Facts and Perspectives

Chen, Haoran; Han, Zhongyu; Wang, Yi; Su, Junyan; Lin, Yumeng; Cheng, Xuhua; Liu, Wen; He, Jingyu; Fan, Yiyue; Chen, Liuyan; Zuo, Houdong

doi:10.2147/jir.s432111

Cited by 13 publications

(5 citation statements)

References 175 publications

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“…Under physiological conditions, cells inhibit lipid peroxidation through several antioxidant systems. The subunit solute carrier family 7 member 11 (SLC7A11)/glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis is a major ferroptosis defense system, and its inactivation can lead to severe ferroptosis ( 58 ). GPX4 is the major lipid peroxide reductase that reduces PL-OOH to nontoxic PL-OH, and its activity is dependent on GSH and selenium ( 59 ).…”

Section: Lncrnas and Ferroptosismentioning

confidence: 99%

“…Extracellular cysteine is transported by the cystine/glutamate reverse transporter (X C -). Its heavy chain SLC7A11 transports extracellular cystine and excretes intracellular glutamate at a 1:1 ratio; subsequently, cystine is reduced to cysteine by NADPH and participates in GSH synthesis ( 58 , 61 ). The SLC7A11-GSH-GPX4 axis constitutes a major PL-OOH detoxification system ( Figure 2 ).…”

Section: Lncrnas and Ferroptosismentioning

confidence: 99%

“…However, during oxidative stress, Nrf2 dissociates from Keap1 and binds to the antioxidant response element (ARE) in the nucleus, thereby activating diverse downstream antioxidant pathways ( 114 ). Nrf2 plays a pivotal role in regulating various ferroptosis-related factors, including GPX4, SLC7A11, and intracellular free iron ( 58 ). The overexpression of the lncRNA LINC01134 is positively associated with a poor prognosis in HCC patients.…”

Section: Ferroptosis-related Lncrnas and Hccmentioning

confidence: 99%

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Ferroptosis and hepatocellular carcinoma: the emerging role of lncRNAs

Chen,

Han,

et al. 2024

Front. Immunol.

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Hepatocellular carcinoma is the most common form of primary liver cancer and poses a significant challenge to the medical community because of its high mortality rate. In recent years, ferroptosis, a unique form of cell death, has garnered widespread attention. Ferroptosis, which is characterized by iron-dependent lipid peroxidation and mitochondrial alterations, is closely associated with the pathological processes of various diseases, including hepatocellular carcinoma. Long non-coding RNAs (lncRNAs), are a type of functional RNA, and play crucial regulatory roles in a variety of biological processes. In this manuscript, we review the regulatory roles of lncRNAs in the key aspects of ferroptosis, and summarize the research progress on ferroptosis-related lncRNAs in hepatocellular carcinoma.

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Section: Lncrnas and Ferroptosismentioning

confidence: 99%

Section: Lncrnas and Ferroptosismentioning

confidence: 99%

Section: Ferroptosis-related Lncrnas and Hccmentioning

confidence: 99%

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Ferroptosis and hepatocellular carcinoma: the emerging role of lncRNAs

Chen,

Han,

et al. 2024

Front. Immunol.

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“…noted that cells with diminished GPX4 expression are more susceptible to ferroptosis, whereas those with elevated GPX4 levels exhibit increased resistance ( 38 ). Consequently, GPX4 serves as a significant regulator of ferroptosis, and modulating its expression can either enhance or suppress the occurrence of ferroptosis ( 16 ).…”

Section: Characteristics Of Ferroptosismentioning

confidence: 99%

Ferroptosis: a novel mechanism of cell death in ophthalmic conditions

Yang,

Lin,

Han

et al. 2024

Front. Immunol.

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Ferroptosis, a new type of programmed cell death proposed in recent years, is characterized mainly by reactive oxygen species and iron-mediated lipid peroxidation and differs from programmed cell death, such as apoptosis, necrosis, and autophagy. Ferroptosis is associated with a variety of physiological and pathophysiological processes. Recent studies have shown that ferroptosis can aggravate or reduce the occurrence and development of diseases by targeting metabolic pathways and signaling pathways in tumors, ischemic organ damage, and other degenerative diseases related to lipid peroxidation. Increasing evidence suggests that ferroptosis is closely linked to the onset and progression of various ophthalmic conditions, including corneal injury, glaucoma, age-related macular degeneration, diabetic retinopathy, retinal detachment, and retinoblastoma. Our review of the current research on ferroptosis in ophthalmic diseases reveals significant advancements in our understanding of the pathogenesis, aetiology, and treatment of these conditions.

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“…Once activated, AMPK orchestrates an intricate cascade that mitigates ATP depletion and bolsters synthesis, thereby reestablishing AMP-ATP balance and ensuring the sustenance of cellular physiological functions. Emerging research posits that AMPK activation engenders Nrf2 (Nuclear factor erythroid 2-related factor 2) activation and nuclear translocation, fortifying cellular antioxidant capacities and impeding ferroptosis (Chen et al, 2023). These findings denote a potential entanglement or confluence of mechanisms between ATP-induced cell demise and ferroptosis, warranting further elucidation.…”

Section: Crosstalk Between Atp Induced Cell Death and Ferroptosismentioning

confidence: 99%

ATP-induced cell death: a novel hypothesis for osteoporosis

Wang,

Zhang,

Sandai

et al. 2023

Front. Cell Dev. Biol.

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ATP-induced cell death has emerged as a captivating realm of inquiry with profound ramifications in the context of osteoporosis. This study unveils a paradigm-shifting hypothesis that illuminates the prospective involvement of ATP-induced cellular demise in the etiology of osteoporosis. Initially, we explicate the morphological attributes of ATP-induced cell death and delve into the intricacies of the molecular machinery and regulatory networks governing ATP homeostasis and ATP-induced cell death. Subsequently, our focus pivots towards the multifaceted interplay between ATP-induced cellular demise and pivotal cellular protagonists, such as bone marrow-derived mesenchymal stem cells, osteoblasts, and osteoclasts, accentuating their potential contributions to secondary osteoporosis phenotypes, encompassing diabetic osteoporosis, glucocorticoid-induced osteoporosis, and postmenopausal osteoporosis. Furthermore, we probe the captivating interplay between ATP-induced cellular demise and alternative modalities of cellular demise, encompassing apoptosis, autophagy, and necroptosis. Through an all-encompassing inquiry into the intricate nexus connecting ATP-induced cellular demise and osteoporosis, our primary goal is to deepen our comprehension of the underlying mechanisms propelling this malady and establish a theoretical bedrock to underpin the development of pioneering therapeutic strategies.

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Targeting Ferroptosis in Bone-Related Diseases: Facts and Perspectives

Cited by 13 publications

References 175 publications

Ferroptosis and hepatocellular carcinoma: the emerging role of lncRNAs

Ferroptosis and hepatocellular carcinoma: the emerging role of lncRNAs

Ferroptosis: a novel mechanism of cell death in ophthalmic conditions

ATP-induced cell death: a novel hypothesis for osteoporosis

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