Genetic factors, including LDL receptor mutations and APOE polymorphisms, interact with environmental factors through epigenetic mechanisms to increase the risk of developing atherosclerosis.
Abstract. Atherosclerosis is one of the most common cardiovascular diseases and a major pathology contributing to increased mortality. This article analyzes the interaction between genetic and environmental factors in the development of atherosclerosis based on current scientific literature. The aim of the study is to identify the combined role of inherent, hereditary characteristics and external environmental factors in predisposing individuals to certain diseases and to assess their interrelationship. The methodological basis involved a comparative analysis of international medical journals, clinical studies, and molecular-genetic research findings. The analysis demonstrates that mutations in the LDL receptor gene, which regulates low-density lipoprotein levels in the blood, and APOE polymorphisms, i.e., small variations at specific locations in the APOE gene that exist among individuals, influence lipid metabolism and thereby modulate the risk of atherosclerosis. Overactivity of the PCSK9 gene disrupts the mechanism controlling LDL cholesterol levels, increasing the likelihood of atherosclerosis. Environmental factors enhance the manifestation of these genetic changes through epigenetic mechanisms, which modify gene expression without altering the DNA sequence. The results highlight the complex etiology of atherosclerosis and emphasize the necessity of considering gene-environment interactions in developing preventive strategies.
Chalaboyeva et al. (Sun,) conducted a review in Atherosclerosis. Genetic predisposition and environmental factors was evaluated on Development of atherosclerosis. Genetic factors, including LDL receptor mutations and APOE polymorphisms, interact with environmental factors through epigenetic mechanisms to increase the risk of developing atherosclerosis.