مشخصات مقاله | |
ترجمه عنوان مقاله | رابطه اصلاح هیستون با ایجاد اسکیزوفرنی |
عنوان انگلیسی مقاله | Association of histone modification with the development of schizophrenia |
نشریه | الزویر |
انتشار | مقاله سال ۲۰۲۴ |
تعداد صفحات مقاله انگلیسی | ۱۱ صفحه |
هزینه | دانلود مقاله انگلیسی رایگان میباشد. |
نوع نگارش مقاله |
مقاله مروری (Review Article) |
مقاله بیس | این مقاله بیس نمیباشد |
نمایه (index) | scopus – master journals List – JCR – MedLine – DOAJ |
نوع مقاله | ISI |
فرمت مقاله انگلیسی | |
ایمپکت فاکتور(IF) |
۷٫۱۹۸ در سال ۲۰۲۲ |
شاخص H_index | ۱۴۹ در سال ۲۰۲۴ |
شاخص SJR | ۱٫۴۹۳ در سال ۲۰۲۲ |
شناسه ISSN | ۱۹۵۰-۶۰۰۷ |
شاخص Quartile (چارک) | Q1 در سال ۲۰۲۲ |
فرضیه | ندارد |
مدل مفهومی | ندارد |
پرسشنامه | ندارد |
متغیر | ندارد |
رفرنس | دارد |
رشته های مرتبط | روانشناسی – پزشکی |
گرایش های مرتبط | روانپزشکی – مغز و اعصاب – روانشناسی بالینی |
نوع ارائه مقاله |
ژورنال |
مجله | زیست پزشکی و دارودرمانی – Biomedicine & Pharmacotherapy |
دانشگاه | School of Forensic Medicine, China Medical University, PR China |
کلمات کلیدی | روانگسیختگی – اصلاح هیستون – بازسازی کروماتین – مقررات رونویسی |
کلمات کلیدی انگلیسی | Schizophrenia – Histone modification – Chromatin remodeling – Transcriptional regulation |
شناسه دیجیتال – doi |
https://doi.org/10.1016/j.biopha.2024.116747 |
لینک سایت مرجع | https://www.sciencedirect.com/science/article/pii/S0753332224006310 |
کد محصول | e17787 |
وضعیت ترجمه مقاله | ترجمه آماده این مقاله موجود نمیباشد. میتوانید از طریق دکمه پایین سفارش دهید. |
دانلود رایگان مقاله | دانلود رایگان مقاله انگلیسی |
سفارش ترجمه این مقاله | سفارش ترجمه این مقاله |
فهرست مطالب مقاله: |
Abstract ۱ Schizophrenia ۲ Histone post-translational modifications Ethical approval Funding sources Authors’ contributions CRediT authorship contribution statement Declaration of Competing Interest Availability of data and materials References |
بخشی از متن مقاله: |
Abstract Schizophrenia, influenced by genetic and environmental factors, may involve epigenetic alterations, notably histone modifications, in its pathogenesis. This review summarizes various histone modifications including acetylation, methylation, phosphorylation, ubiquitination, serotonylation, lactylation, palmitoylation, and dopaminylation, and their implications in schizophrenia. Current research predominantly focuses on histone acetylation and methylation, though other modifications also play significant roles. These modifications are crucial in regulating transcription through chromatin remodeling, which is vital for understanding schizophrenia’s development. For instance, histone acetylation enhances transcriptional efficiency by loosening chromatin, while increased histone methyltransferase activity on H3K9 and altered histone phosphorylation, which reduces DNA affinity and destabilizes chromatin structure, are significant markers of schizophrenia.
Schizophrenia Schizophrenia is a complex, heterogeneous psychiatric disorder influenced by both genetic and environmental factors, with a lifetime prevalence of approximately 1 % in the general population [1] . This condition manifests through a spectrum of symptoms: (i) positive symptoms such as delusions, hallucinations, paranoia, thought disorders, and psychomotor agitation; (ii) negative symptoms including emotional blunting, social withdrawal, and deficits in motivation and reward processing; (iii) cognitive impairment affecting learning, attention, executive function, and memory, particularly working memory [2] , [3] . Mood disturbances such as depression and anxiety are also common among patients.
The pathogenesis of schizophrenia is currently explained by several theories, the most notable being the dopaminergic hypothesis. This hypothesis proposes that positive symptoms arise from dysregulated dopaminergic neurotransmission in the limbic system of the midbrain, while disruptions in cortical pathways contribute to negative symptoms [4] . The glutamatergic hypothesis posits that changes in NMDA receptor-mediated glutamatergic transmission affect prefrontal neuronal connectivity [5] , and the serotonergic hypothesis attributes disturbances in neuronal activity to serotonin overload from the dorsal raphe nucleus serotonergic hypothesis suggests that stress causes overload of serotonin from the dorsal raphe nucleus [6] . The GABAergic hypothesis suggests that an imbalance between cortical excitation and inhibition, driven by disruptions in GABAergic neurotransmission, underlies the disorder [7] . Additionally, nicotinic receptors play a role in cholinergic transmission; studies have shown that nicotine can improve attention and memory performance in schizophrenic patients [8] . Cognitive dysfunction, a core feature observed in over 80 % of individuals with schizophrenics, involves multiple brain regions, including the dorsolateral and medial prefrontal cortices and the parietal regions [9] , [10] , [11] . Structural abnormalities in the medial temporal lobe, particularly the hippocampus, have been linked to memory deficits and play a significant role in the neural networks responsible for memory and spatial navigation [12] , [13] , [14] , [15] , [16] . |