Identification of lncRNA-miRNA-mRNA Networks in the Lenticular Nucleus Region of the Brain Contributes to Hepatolenticular Degeneration Pathogenesis and Therapy

Hao, Wenjie; Yang, Wenming; Yang, Yue; Cheng, Ting; Wei, Taohua; Tang, Lulu; Qian, Nannan; Yang, Yulong; Li, Xiang; Jiang, Hailin; Wang, Meixia

doi:10.1007/s12035-023-03631-1

Cited by 3 publications

(1 citation statement)

References 77 publications

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“…For example, the methylation levels of SORBS3 , solute carrier family 2A ( SLC2A4 ), and other genes decrease, while those of Ankyrin 1 ( ANK1 ), rhomboid 5 homolog 2 ( RHBDF2 ), and other genes increase [ 54 ]. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses have indicated that these dysregulated methylated genes are enriched in pathways related to synaptic transmission, long-term potentiation, and psychiatric disorders [ 57 ].…”

Section: Dna Methylation and Pathogenesis Of Admentioning

confidence: 99%

An Epigenetic Manifestation of Alzheimer's Disease: DNA Methylation

Feng,

Zheng,

Cai

et al. 2024

Actas Esp Psiquiatr

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Alzheimer's disease (AD), the most common form of dementia, has a complex pathogenesis. The number of AD patients has increased in recent years due to population aging, while a trend toward a younger age of onset has arisen, imposing a substantial burden on society and families, and garnering extensive attention. DNA methylation has recently been revealed to play an important role in AD onset and progression. DNA methylation is a critical mechanism regulating gene expression, and alterations in this mechanism dysregulate gene expression and disrupt important pathways, including oxidative stress responses, inflammatory reactions, and protein degradation processes, eventually resulting in disease. Studies have revealed widespread changes in AD patients' DNA methylation in the peripheral blood and brain tissues, affecting multiple signaling pathways and severely impacting neuronal cell and synaptic functions. This review summarizes the role of DNA methylation in the pathogenesis of AD, aiming to provide a theoretical basis for its early prevention and treatment.

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Section: Dna Methylation and Pathogenesis Of Admentioning

confidence: 99%

An Epigenetic Manifestation of Alzheimer's Disease: DNA Methylation

Feng,

Zheng,

Cai

et al. 2024

Actas Esp Psiquiatr

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Non‐Coding RNA in Schwann Cell and Peripheral Nerve Injury: A Review

Huang,

Sun,

Sun

et al. 2024

Advanced Biology

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Peripheral nerve injury (PNI) can result in severe disabilities, profoundly impacting patients' quality of life and potentially endangering their lives. Therefore, understanding the potential molecular mechanisms that facilitate the regeneration of damaged nerves is crucial. Evidence indicates that Schwann cells (SCs) play a pivotal role in repairing peripheral nerve injuries. Previous studies have shown that RNA, particularly non‐coding RNA (ncRNA), plays a crucial role in nerve regeneration, including the proliferation and dedifferentiation of SCs. In this review, the individual roles of ncRNA in SCs and PNI are analyzed. This review not only enhances the understanding of ncRNA's role in nerve injury repair but also provides a significant theoretical foundation and inspiration for the development of new therapeutic strategies.

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Psychiatric Symptoms in Wilson’s Disease—Consequence of ATP7B Gene Mutations or Just Coincidence?—Possible Causal Cascades and Molecular Pathways

Gromadzka,

Antos,

Sorysz

et al. 2024

IJMS

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Wilson’s disease (WD) is an autosomal recessive disorder of copper metabolism. The genetic defect in WD affects the ATP7B gene, which encodes the ATP7B transmembrane protein, which is essential for maintaining normal copper homeostasis in the body. It is primarily expressed in the liver and acts by incorporating copper into ceruloplasmin (Cp), the major copper transport protein in the blood. In conditions of excess copper, ATP7B transports it to bile for excretion. Mutations in ATP7B lead to impaired ATP7B function, resulting in copper accumulation in hepatocytes leading to their damage. The toxic “free”—unbound to Cp—copper released from hepatocytes then accumulates in various organs, contributing to their damage and clinical manifestations of WD, including hepatic, neurological, hematological, renal, musculoskeletal, ophthalmological, psychiatric, and other effects. While most clinical manifestations of WD correspond to identifiable organic or cellular damage, the pathophysiology underlying its psychiatric manifestations remains less clearly understood. A search for relevant articles was conducted in PubMed/Medline, Science Direct, Scopus, Willy Online Library, and Google Scholar, combining free text and MeSH terms using a wide range of synonyms and related terms, including “Wilson’s disease”, “hepatolenticular degeneration”, “psychiatric manifestations”, “molecular mechanisms”, “pathomechanism”, and others, as well as their combinations. Psychiatric symptoms of WD include cognitive disorders, personality and behavioral disorders, mood disorders, psychosis, and other mental disorders. They are not strictly related to the location of brain damage, therefore, the question arises whether these symptoms are caused by WD or are simply a coincidence or a reaction to the diagnosis of a genetic disease. Hypotheses regarding the etiology of psychiatric symptoms of WD suggest a variety of molecular mechanisms, including copper-induced CNS toxicity, oxidative stress, mitochondrial dysfunction, mitophagy, cuproptosis, ferroptosis, dysregulation of neurotransmission, deficiencies of neurotrophic factors, or immune dysregulation. New studies on the expression of noncoding RNA in WD are beginning to shed light on potential molecular pathways involved in psychiatric symptomatology. However, current evidence is still insufficient to definitively establish the cause of psychiatric symptoms in WD. It is possible that the etiology of psychiatric symptoms varies among individuals, with multiple biological and psychological mechanisms contributing to them simultaneously. Future studies with larger samples and comprehensive analyses are necessary to elucidate the mechanisms underlying the psychiatric manifestations of WD and to optimize diagnostics and therapeutic approaches.

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Identification of lncRNA-miRNA-mRNA Networks in the Lenticular Nucleus Region of the Brain Contributes to Hepatolenticular Degeneration Pathogenesis and Therapy

Cited by 3 publications

References 77 publications

An Epigenetic Manifestation of Alzheimer's Disease: DNA Methylation

An Epigenetic Manifestation of Alzheimer's Disease: DNA Methylation

Non‐Coding RNA in Schwann Cell and Peripheral Nerve Injury: A Review

Psychiatric Symptoms in Wilson’s Disease—Consequence of ATP7B Gene Mutations or Just Coincidence?—Possible Causal Cascades and Molecular Pathways

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