Role of Imprinted Genes in Multiple Sclerosis Pathogenesis
Multiple sclerosis (MS) is a chronic autoimmune neurodegenerative disease of the central nervous system characterized by inflammation, demyelination, and neuronal damage. Recent advances in genomics and epigenetics have shed light on the complex interplay between genetic factors and environmental triggers in the pathogenesis of MS. Among the genetic factors, imprinted genes have emerged as significant contributors to MS pathogenesis.
Imprinted Genes and Their Role in MS
Genomic imprinting is an epigenetic mechanism that results in the monoallelic expression of genes depending on their parental origin. This phenomenon can influence various biological processes, including development, metabolism, and immune responses. Recent studies have suggested that disturbances in imprinted genes may play a role in the development of MS.
Imprinted Genes and MS Pathogenesis: A study by Baulina et al. (2021) reviews the potential involvement of imprinted genes in MS pathogenesis. The authors discuss how epigenetic mechanisms, including genomic imprinting, could link genetic and non-genetic risk factors for MS. They emphasize the need for extensive research on epigenetics to unravel MS molecular mechanisms, suggesting that disturbances in imprinted genes may affect their expression in MS and contribute to disease development.
Epigenetic Insights into MS Progression: Kular and Jagodic (2020) provide a comprehensive review of the role of epigenetics in MS progression. They discuss how DNA and histone modifications could impair oligodendrocyte differentiation and myelination processes, contributing to MS. The review highlights the potential of epigenetic insights to unravel mechanisms underlying MS progression and suggests avenues for future treatments.
The Imprintome and Human Diseases: Jima et al. (2022) discuss the establishment of a draft human imprintome, identifying candidate imprint control regions (ICRs) through whole-genome bisulphite sequencing. This genomic map could facilitate the investigation of the developmental origins of diseases, including MS, by examining epigenetic dysregulation in accessible tissues. The study underscores the importance of understanding imprinting dysregulation in the pathogenesis of human diseases.
Conclusion
The emerging research on imprinted genes and their epigenetic regulation offers new perspectives on the pathogenesis of MS. These studies highlight the complexity of MS development, involving both genetic predispositions and environmental influences. By deepening our understanding of epigenetic mechanisms like genomic imprinting, researchers can pave the way for novel therapeutic targets and strategies to combat MS. The integration of epigenetics into the study of MS holds promise for uncovering the molecular underpinnings of the disease and improving patient outcomes.
Reference:
Baulina, N., Kiselev, I., & Favorova, O. (2021). Imprinted Genes and Multiple Sclerosis: What Do We Know?. International Journal of Molecular Sciences, 22.
Kular, L., & Jagodic, M. (2020). Epigenetic insights into multiple sclerosis disease progression. Journal of Internal Medicine, 288, 102 - 82.
Jima, D., Skaar, D., Planchart, A., Motsinger-Reif, A., Çevik, Ş., Park, S., Cowley, M., Wright, F., House, J., Liu, A., Jirtle, R., & Hoyo, C. (2022). Genomic map of candidate human imprint control regions: the imprintome. Epigenetics, 17, 1920 - 1943.