International Journal of Molecular Sciences

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The Role of Epigenetics in Genome Maintenance and Its Relationship to Organismal Aging and Age-Related Diseases

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Dr. Berta Vázquez

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Guest Editor

1. Cell Biology, Physiology and Immunology Department, Autonomous University of Barcelona, 080193 Bellaterra, Spain
2. Chromatin Biology Laboratory, Josep Carreras Leukaemia Research Institute (IJC), Ctra de Can Ruti, Camí de les Escoles s/n, 08916 Badalona, Barcelona, Spain
Interests: genome integrity; chromatin; epigenetics; aging; meiosis; differentiation; cancer; neurodegeneration; inflammation

Dr. Gerardo Ferrer

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Guest Editor

1. Cancer Epigenetics, Josep Carreras Leukaemia Research Institute (IJC), Badalona, Spain
2. Karches Center for Oncology Research, The Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, USA
3. Centro de Investigación Biomédica en Red Cáncer (CIBERONC), Madrid, Spain
Interests: myelodysplastic syndrome; leukaemia

Special Issue Information

Dear Colleagues,

The maintenance of genome integrity is an intricate process involving the coordination of DNA repair, replication, transcription, and chromosome segregation pathways. These processes occur within the immensely complex environment of chromatin and require the action of multiple epigenetic factors. Despite the importance of chromatin regulation in maintaining genome integrity, researchers do not fully understand the mechanisms of action and their contributions to human diseases.

Chromatin regulation is particularly crucial in the context of aging. Epigenetic signatures, such as DNA methylation, histone modifications, and chromatin remodeling, undergo various changes as organisms age. These changes impact genome stability with significant consequences for human health, including a decline in reproductive capabilities and the appearance of age-related diseases such as cancer, neurodegeneration, and inflammatory conditions. Importantly, there is great clinical interest in targeting epigenetic proteins as they can reverse abnormal epigenetic information and restore genome function.

In this Special Issue, we invite researchers to present original studies and state-of-the-art reviews on epigenetic mechanisms. By discussing their data and opinions, researchers can provide valuable insights into the complex interactions between chromatin dynamics, genome integrity, aging, and disease.

Dr. Berta Vázquez
Dr. Gerardo Ferrer
Guest Editors

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18 pages, 4065 KiB

Open AccessArticle

Effects of Astragaloside IV and Formononetin on Oxidative Stress and Mitochondrial Biogenesis in Hepatocytes

by Quoc-Anh Tran, Grant Van Tran, Sanel Velic, Hou-Mai Xiong, Jaspreet Kaur, Zuhurr Moosavi, Phuong Nguyen, Nhi Duong, Vy Tran Luu, Gurjot Singh, Tram Bui, Melanie Rose and Linh Ho

Int. J. Mol. Sci. 2025, 26(2), 774; https://doi.org/10.3390/ijms26020774 - 17 Jan 2025

Cited by 2 | Viewed by 1007

Abstract

Over-accumulation of reactive oxygen species (ROS) causes hepatocyte dysfunction and apoptosis that might lead to the progression of liver damage. Sirtuin-3 (SIRT3), the main NAD+-dependent deacetylase located in mitochondria, has a critical role in regulation of mitochondrial function and ROS production as well as in the mitochondrial antioxidant mechanism. This study explores the roles of astragaloside IV (AST-IV) and formononetin (FMR) in connection with SIRT3 for potential antioxidative effects. It was shown that the condition of combined pre- and post-treatment with AST-IV or FMR at all concentrations statistically increased and rescued cell proliferation. ROS levels were not affected by pre-or post-treatment individually with AST-IV or pre-treatment with FMR; however, post-treatment with FMR resulted in significant increases in ROS in all groups. Significant decreases in ROS levels were seen when pre- and post-treatment with AST-IV were combined at 5 and 10 μM, or FMR at 5 and 20 μM. In the condition of combined pre- and post-treatment with 10 μM AST-IV, there was a significant increase in SOD activity, and the transcriptional levels of Sod2, Cat, and GPX1 in all treatment groups, which is indicative of reactive oxygen species detoxification. Furthermore, AST-IV and FMR activated PGC-1α and AMPK as well as SIRT3 expression in AML12 hepatocytes exposed to t-BHP-induced oxidative stress, especially at high concentrations of FMR. This study presents a novel mechanism whereby AST-IV and FMR yield an antioxidant effect through induction of SIRT3 protein expression and activation of an antioxidant mechanism as well as mitochondrial biogenesis and mitochondrial content and potential. The findings suggest these agents can be used as SIRT3 modulators in treating oxidative-injury hepatocytes. Full article

(This article belongs to the Special Issue The Role of Epigenetics in Genome Maintenance and Its Relationship to Organismal Aging and Age-Related Diseases)

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