Increased m6A modification of BDNF mRNA via FTO promotes neuronal apoptosis following aluminum-induced oxidative stress

Song, Jing; Hao, Jiarui; Lu, Yang; Ding, Xiaohui; Li, Mujia; Xin, Yulu

doi:10.1016/j.envpol.2024.123848

Cited by 3 publications

(2 citation statements)

References 41 publications

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“…Epigenetic alterations influenced by variables like age and environment may also influence the advancement of HCC related to MASLD. A growing body of proof has indicated that epigenetic modifications, including DNA methylation, histone modification, RNA modification, and non-coding RNA (ncRNA)-mediated processes, are significantly linked with the progression of MASLD and HCC [ 36 , 37 ].…”

Section: Masld-induced Hccmentioning

confidence: 99%

Crosstalk between Epigenetics and Metabolic Reprogramming in Metabolic Dysfunction-Associated Steatotic Liver Disease-Induced Hepatocellular Carcinoma: A New Sight

Li,

Wang,

Zhao

et al. 2024

Metabolites

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Epigenetic and metabolic reprogramming alterations are two important features of tumors, and their reversible, spatial, and temporal regulation is a distinctive hallmark of carcinogenesis. Epigenetics, which focuses on gene regulatory mechanisms beyond the DNA sequence, is a new entry point for tumor therapy. Moreover, metabolic reprogramming drives hepatocellular carcinoma (HCC) initiation and progression, highlighting the significance of metabolism in this disease. Exploring the inter-regulatory relationship between tumor metabolic reprogramming and epigenetic modification has become one of the hot directions in current tumor metabolism research. As viral etiologies have given way to metabolic dysfunction-associated steatotic liver disease (MASLD)-induced HCC, it is urgent that complex molecular pathways linking them and hepatocarcinogenesis be explored. However, how aberrant crosstalk between epigenetic modifications and metabolic reprogramming affects MASLD-induced HCC lacks comprehensive understanding. A better understanding of their linkages is necessary and urgent to improve HCC treatment strategies. For this reason, this review examines the interwoven landscape of molecular carcinogenesis in the context of MASLD-induced HCC, focusing on mechanisms regulating aberrant epigenetic alterations and metabolic reprogramming in the development of MASLD-induced HCC and interactions between them while also updating the current advances in metabolism and epigenetic modification-based therapeutic drugs in HCC.

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Section: Masld-induced Hccmentioning

confidence: 99%

Crosstalk between Epigenetics and Metabolic Reprogramming in Metabolic Dysfunction-Associated Steatotic Liver Disease-Induced Hepatocellular Carcinoma: A New Sight

Li,

Wang,

Zhao

et al. 2024

Metabolites

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“…Various neurotoxins, such as perfluorooctane sulfonate (PFOS), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), and domoic acid, can trigger neuronal damage ( Gratuze et al, 2019 ; Wu et al, 2019 ; Petroff et al, 2022 ; Figure 1 ). In particular, aluminum, is known to induce severe cognitive deficits through persistent oxidative stress, increased N6-methyladenosine modification of brain-derived neurotrophic factor mRNA, and promotion of neuronal apoptosis ( Song et al, 2024 ; Figure 1 ). Additionally, exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) has been linked to cerebral and cognitive impairments, with TCDD activating caspase-3 and leading to extensive neuronal apoptosis ( Xu et al, 2014 ; Figure 1 ).…”

Section: The Role Of Neuron In Coimentioning

confidence: 99%

The role of Foxo3a in neuron-mediated cognitive impairment

Liu,

Wu,

Wang

et al. 2024

Front. Mol. Neurosci.

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Cognitive impairment (COI) is a prevalent complication across a spectrum of brain disorders, underpinned by intricate mechanisms yet to be fully elucidated. Neurons, the principal cell population of the nervous system, orchestrate cognitive processes and govern cognitive balance. Extensive inquiry has spotlighted the involvement of Foxo3a in COI. The regulatory cascade of Foxo3a transactivation implicates multiple downstream signaling pathways encompassing mitochondrial function, oxidative stress, autophagy, and apoptosis, collectively affecting neuronal activity. Notably, the expression and activity profile of neuronal Foxo3a are subject to modulation via various modalities, including methylation of promoter, phosphorylation and acetylation of protein. Furthermore, upstream pathways such as PI3K/AKT, the SIRT family, and diverse micro-RNAs intricately interface with Foxo3a, engendering alterations in neuronal function. Through several downstream routes, Foxo3a regulates neuronal dynamics, thereby modulating the onset or amelioration of COI in Alzheimer’s disease, stroke, ischemic brain injury, Parkinson’s disease, and traumatic brain injury. Foxo3a is a potential therapeutic cognitive target, and clinical drugs or multiple small molecules have been preliminarily shown to have cognitive-enhancing effects that indirectly affect Foxo3a. Particularly noteworthy are multiple randomized, controlled, placebo clinical trials illustrating the significant cognitive enhancement achievable through autophagy modulation. Here, we discussed the role of Foxo3a in neuron-mediated COI and common cognitively impaired diseases.

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Role of reactive oxygen species in regulating epigenetic modifications

Chen,

Shen

2025

Cellular Signalling

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Increased m6A modification of BDNF mRNA via FTO promotes neuronal apoptosis following aluminum-induced oxidative stress

Cited by 3 publications

References 41 publications

Crosstalk between Epigenetics and Metabolic Reprogramming in Metabolic Dysfunction-Associated Steatotic Liver Disease-Induced Hepatocellular Carcinoma: A New Sight

Crosstalk between Epigenetics and Metabolic Reprogramming in Metabolic Dysfunction-Associated Steatotic Liver Disease-Induced Hepatocellular Carcinoma: A New Sight

The role of Foxo3a in neuron-mediated cognitive impairment

Role of reactive oxygen species in regulating epigenetic modifications

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