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Epigenetic miRNA Mediated Regulation of RAS in Cardiovascular Diseases

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The Renin Angiotensin System in Cardiovascular Disease

Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 24))

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Abstract

The renin angiotensin system (RAS) is well-known for its function in blood pressure regulation and its association with numerous cardiovascular diseases (CVDs). Dysregulation of the RAS can result in hypertension, subsequently promoting cardiovascular disorders, including hypertrophy, cardiac fibrosis, and heart failure. During the Coronavirus disease 2019 (COVID-19) pandemic, further functions of the RAS came to attention, as it was associated with the viral entry. Moreover, the RAS has always been of great research interest due to its importance in physiology. Advances in research have revealed that in addition to the canonical RAS, several organs, for instance, the heart, appear to have their own local RAS. Furthermore, technical advances have led to the discovery of new RAS components and a greater understanding of their interactions and epigenetic regulation. Several mechanisms are associated with epigenetics, including histone modification, DNA methylation, and non-coding RNAs (ncRNAs) such as microRNAs (miRNAs). The role of epigenetic modifications and miRNAs has been of great research interest since miRNAs and their possible functions were discovered. In addition to established laboratory methods, new methods such as next-generation sequencing and bioinformatics provide the necessary tools for finding novel miRNAs with therapeutic value as biomarkers of disease or potential medication. Thus, we aim to give a brief overview of RAS-related miRNAs and their impact on CVDs.

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Caliskan, A., Crouch, S.A.W., Dangwal, S. (2023). Epigenetic miRNA Mediated Regulation of RAS in Cardiovascular Diseases. In: Dhalla, N.S., Bhullar, S.K., Shah, A.K. (eds) The Renin Angiotensin System in Cardiovascular Disease. Advances in Biochemistry in Health and Disease, vol 24. Springer, Cham. https://doi.org/10.1007/978-3-031-14952-8_5

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