Unravelling the role of NFE2L1 in stress responses and related diseases

Liu, Xingzhu; Xu, Chunping; Xiao, Wanglong; Yan, Nianlong

doi:10.1016/j.redox.2023.102819

Cited by 13 publications

(5 citation statements)

References 198 publications

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“…Previous studies have indicated that AT accumulation in the mesentery is accompanied by inflammation. Although there are a limited number of studies that explore NFE2L1 expression as a direct cause of Crohn's disease, its typical genetic association and functional significance in other IBDs suggest that it may play an important role [56,57]. The expression levels of lncRNA G8110 and NFE2L1 were decreased in the WG group, and lncRNA G8110 showed beneficial effects by promoting lipid metabolism and inhibiting adipose inflammation (Figure 4).…”

Section: Discussionmentioning

confidence: 99%

Identification of a Novel Long Non-Coding RNA G8110 That Modulates Porcine Adipogenic Differentiation and Inflammatory Responses

Chai,

Wang,

Chen

et al. 2023

IJMS

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Long non-coding RNAs (lncRNAs) have been extensively studied, and their crucial roles in adipogenesis, lipid metabolism, and gene expression have been revealed. However, the exact regulatory or other mechanisms by which lncRNAs influence the functioning of mesenteric adipose tissue (MAT) remain largely unknown. In this paper, we report the identification of a new lncRNA, named G8110, from the MAT of Bama pigs. The coordinated expression levels of lncRNA G8110 and NFE2L1 were significantly decreased in the MAT of obese Bama pigs compared with those in the MAT of lean pigs. Using a bone mesenchymal stem cell adipogenic differentiation model, we found that lncRNA G8110 played a role in adipocyte differentiation by positively regulating NFE2L1. We also found that lncRNA G8110 inhibited the formation of intracellular lipid synthesis, promoted lipid metabolism, and inhibited the expression of inflammatory cytokines. Our findings regarding lipid synthesis may further promote the role of lncRNAs in driving adipose tissue remodeling and maintaining metabolic health.

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Section: Discussionmentioning

confidence: 99%

Identification of a Novel Long Non-Coding RNA G8110 That Modulates Porcine Adipogenic Differentiation and Inflammatory Responses

Chai,

Wang,

Chen

et al. 2023

IJMS

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“…However, the appeal of NFE2L1-related cellular and molecular mechanisms consists in different isoforms and SNPs, which are still under investigation. Recently, NFE2L1-related isoforms and SNPs serve as potential therapeutical targets for neurodegenerative diseases [163] and cancer [164], and are receiving increased attention. The value of NFE2L1 for developing precise cancer treatment is immeasurable.…”

Section: Discussionmentioning

confidence: 99%

Understanding the Transcription Factor NFE2L1/NRF1 from the Perspective of Hallmarks of Cancer

Zhang,

Liu,

Zhang

et al. 2024

Antioxidants

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Cancer cells subvert multiple properties of normal cells, including escaping strict cell cycle regulation, gaining resistance to cell death, and remodeling the tumor microenvironment. The hallmarks of cancer have recently been updated and summarized. Nuclear factor erythroid 2-related factor 1 (NFE2L1, also named NRF1) belongs to the cap’n’collar (CNC) basic-region leucine zipper (bZIP) family. It acts as a transcription factor and is indispensable for maintaining both cellular homoeostasis and organ integrity during development and growth, as well as adaptive responses to pathophysiological stressors. In addition, NFE2L1 mediates the proteasome bounce-back effect in the clinical proteasome inhibitor therapy of neuroblastoma, multiple myeloma, and triple-negative breast cancer, which quickly induces proteasome inhibitor resistance. Recent studies have shown that NFE2L1 mediates cell proliferation and metabolic reprogramming in various cancer cell lines. We combined the framework provided by “hallmarks of cancer” with recent research on NFE2L1 to summarize the role and mechanism of NFE2L1 in cancer. These ongoing efforts aim to contribute to the development of potential novel cancer therapies that target the NFE2L1 pathway and its activity.

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“…A growing body of evidence reveals that Nrf1 plays a crucial role in regulating intracellular metabolism [29,67,68], because the loss of its function leads to marked metabolic signal reprogramming [67,[69][70][71]. In this process, Nrf1 exerts its unique indispensable functions for governing the intracellular redox and energy (including lipid, cholesterol, glucose) metabolic homeostasis and also maintaining protein homeostasis and even chromosomal stability [20,22,31].…”

Section: The Loss Of Nrf1 Exacerbates Development Of Sasp By Reprogra...mentioning

confidence: 99%

“…The accumulating evidence has suggested that impaired Nrf1 function is much more likely to trigger the occurrence and progression of ageing-related pathologies (e.g., cardiovascular diseases, inflammatory diseases, neurodegenerative diseases), which are evidenced to be closely associated with compromised adaptive responses (i.e., both responses to oxidative and proteotoxic stresses monitored by Nrf1). Conversely, either pharmacological or phytochemical agents that promote Nrf1 activation demonstrated a considerable promise to act as potential targets for the prevention or treatment of age-related disorders [20,29]. Thereby, it is inferable that, as a key regulator of the antioxidant system, Nrf1 has shown its significant potential in protecting cells and organisms from cellular senescence and ageing.…”

Section: Introductionmentioning

confidence: 99%

Deletion of Nrf1 exacerbates oxidative stress-induced cellular senescence by disrupting the cell homeostasis

Lyu,

Wang,

Qiu

et al. 2024

Preprint

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Nuclear factor erythroid-derived 2-like 1(Nrf1,encoded by Nfe2l1), an essential transcription factor of the cap'n'collar basic-region leucine zipper(CNC-bZIP)family, is highly conserved with its homologous Nuclear factor erythroid-derived 2-like 2(Nrf2,encoded by Nfe2l2). Of note, Nrf1 possesses a remarkable anti-senescence potential, but it has not been comprehensively characterized to date. Conversely, Nrf1α-/- cells undergoing senescence display hallmarks of senescence, comprising heightened activity of senescence-associated β-galactosidase, decreased cell vitality, cell growth arrest, and increased expression of the senescence-associated secretory phenotype. Further investigation showed cellular senescence in Nrf1α-/- cells is not a consequence of Nrf2 accumulation. On the contrary, Nrf2 could alleviate, but not halt or reverse, senescence of Nrf1α-/- cells. This is predominantly attributable to the fact that, different from Nrf2, the deficiency of Nrf1 brings about activation of both p21 and RB pathwanys independently of p53, but disrupts STAG2- and SMC3-dependent chromosomal homeostasis so to drive cell senescence. Here, we discover the significant anti-senescence capacity of Nrf1 and highlight two mechanisms underlying the protective function of Nrf1, which stem from its response to stress and its role in maintaining cellular homeostasis.

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Unravelling the role of NFE2L1 in stress responses and related diseases

Cited by 13 publications

References 198 publications

Identification of a Novel Long Non-Coding RNA G8110 That Modulates Porcine Adipogenic Differentiation and Inflammatory Responses

Identification of a Novel Long Non-Coding RNA G8110 That Modulates Porcine Adipogenic Differentiation and Inflammatory Responses

Understanding the Transcription Factor NFE2L1/NRF1 from the Perspective of Hallmarks of Cancer

Deletion of Nrf1 exacerbates oxidative stress-induced cellular senescence by disrupting the cell homeostasis

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