Numerous genetic and environmental factors contribute to neurodegenerative diseases characterized by damage to the DNA and changes in the chromatin structure. Many studies have shown that DNA damage and chromatin organization are closely linked, but more research is needed to fully understand this connection, especially in neurodegenerative diseases. Important proteins implicated in neurodegenerative disorders have been linked to chromatin reconfiguration and DNA damage, according to recent research. Epigenetic interventions such as HDAC inhibitors approved for cancer therapy, can be repurposed for neurodegenerative diseases. Furthermore, microRNAs, often dysregulated in neurodegenerative conditions, could be targeted to restore normal gene regulation. Exploring these strategies could lead to more effective treatments by addressing the fundamental epigenetic and chromatin-related mechanisms involved in neurodegeneration. This review discusses the relationship between the contributing proteins and various neurodegenerative diseases, with particular attention to key proteins like tau, which is associated with microtubules, superoxide dismutase 1, huntingtin, α-synuclein, β-amyloid precursor protein and TAR DNA/RNA binding protein 43 and their role in DNA protection and damage repair.
Hypertrophic cardiomyopathy (HCM) is a monogenic cardiovascular disorder that has been poorly studied at the molecular, genetic, and computational levels. Here, we examined the genetic map of HCM polymorphic targets using a computational approach to identify new phytochemicals with potential therapeutic properties. We demonstrate the range of mutations associated with cardiomyopathies, and identify new associations between genes and phenotypes in this disease category. Specifically, our findings suggest that several genes associated with channelopathies might serve as genetic modifiers, altering the clinical features and severity of cardiomyopathic phenotypes, thus likely impacting disease manifestation.
To study the potential molecular mechanism of chrysin in treating HSV-1 based on network pharmacology.
The targets of chrysin were predicted using the SEA, Swiss, and PharmMapper databases, and HSV-1 infection-related genes were identified from the NCBI and Genecard databases. A protein-protein interaction (PPI) network was constructed using Cytoscape 3.9.1 with these genes, followed by GO enrichment and KEGG pathway analyses. Molecular docking was employed to analyze the interaction sites using the AutoDock Vina algorithm.
Network pharmacology analysis identified 178 potential targets associated with chrysin treatment of HSV. Moreover, 2029 HSV-1-related genes were identified, 43 of which were overlapped with chrysin treatment targets. Additionally, 358 GO entries were identified, encompassing 255 biological processes (BP), 38 molecular functions (MF), and 65 cell components (CC). Molecular docking simulations were conducted to assess the binding affinity between chrysin and the predicted hub genes (SRC, VEGFA, EGFR, PTGS2, CDK1, AR, PARP1, and ABL1).
In this study, a potential molecular target of chrysin action in combating HSV-1 infection was identified, offering a novel approach to enhancing the antiviral effectiveness in patients with HSV-1 infection.