Role of SNP markers on chromosome 10 in the pathogenesis of atrial fibrillation

Abstract. Introduction. Studying genetic factors favoring atrial fibrillation not only contributes to the expansion of our knowledge about the causes of the disease, but also opens up opportunities for the individualized prediction of its development. Increased attention to the genetic aspects of atrial fibrillation is primarily due to the lack of knowledge about the etiology and pathogenesis of atrial fibrillation and the annual increase in the number of patients diagnosed with this disease. Aim. Analyzing the studies on the influence of SNP markers on chromosome 10 upon the pathogenesis of atrial fibrillation. Materials and Methods. Analysis of scientific publications on the influence of SNP markers on chromosome 10 upon the pathogenesis of atrial fibrillation. Results and Discussion. When studying the genetic component in the pathology of atrial fibrillation, it was found that most (more than 11) SNP markers are located on chromosome 10. Each of them encodes proteins involved in the process of contraction and/or impulse transmission. The most well-studied genes are MYOZ1 encoding the protein myozenin 1 involved in calcineurin signal transduction and interacting with proteins on the Z-disc of the cardiac sarcomere, including α-actinin and γ-filamin; and SYNPO2L, a gene that encodes the protein sequence synaptopodin 2 acting as a hub protein involved in arranging and anchoring actin in the cell, and potentially necessary for the correct localization of α-actinin. Genes NEURL, associated with PITX2, VCL, and Cav1 and Syne2, the functional role of which remains unclear to this day, are also involved in the development of atrial fibrillation. Conclusions. One of the etiological factors in the development of atrial fibrillation is a genetic predisposition associated with genes located on chromosome 10, which encode proteins that are part of sarcomeres or represent signaling molecules in impulse transmission in the heart.