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1.
Curr Mol Med ; 23(10): 1012-1027, 2023.
Artigo em Inglês | MEDLINE | ID: mdl-36200195

RESUMO

Epigenetic modifications play a vital role in gene regulation associated with different pathologies. Various nutrients in our diet, such as vitamins can modulate these epigenetic mechanism. They also can regulatenderlying pathophysiological factors and processes that directly or indirectly. Most importantly, A, B, C, and D vitamins have recently been shown to be involved in this type of regulation together with vitamins E and K. Despite their effect on the DNA methylation process, an in-depth understanding of vitamin-mediated epigenetic alterations have yet to be investigated. Moreover, the role of vitamins in DNA methylation as nutraceuticals might be important to use for targeted therapy of various human diseases. Overall, this review provides a brief survey of the role of vitamins as epigenetic modulators or nutraceuticals, emphasizing their potential in epigenetic therapy.


Assuntos
Metilação de DNA , Vitaminas , Humanos , Vitaminas/farmacologia , Suplementos Nutricionais , Vitamina A , Vitamina K , Epigênese Genética
2.
Biomolecules ; 12(10)2022 Oct 10.
Artigo em Inglês | MEDLINE | ID: mdl-36291661

RESUMO

Alzheimer's disease (AD) is considered a chronic and debilitating neurological illness that is increasingly impacting older-age populations. Some proteins, including clusterin (CLU or apolipoprotein J) transporter, can be linked to AD, causing oxidative stress. Therefore, its activity can affect various functions involving complement system inactivation, lipid transport, chaperone activity, neuronal transmission, and cellular survival pathways. This transporter is known to bind to the amyloid beta (Aß) peptide, which is the major pathogenic factor of AD. On the other hand, this transporter is also active at the blood-brain barrier (BBB), a barrier that prevents harmful substances from entering and exiting the brain. Therefore, in this review, we discuss and emphasize the role of the CLU transporter and CLU-linked molecular mechanisms at the BBB interface in the pathogenesis of AD.


Assuntos
Doença de Alzheimer , Clusterina , Humanos , Clusterina/metabolismo , Doença de Alzheimer/metabolismo , Peptídeos beta-Amiloides/metabolismo , Barreira Hematoencefálica/metabolismo , Proteínas de Membrana Transportadoras/metabolismo , Lipídeos
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