الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Spondylarthritis (SpA) arises from a combination of genetic susceptibility and environmental influences. The presence of a crucial genetic element, mostly influenced by the major histocompatibility complex allele HLA-B27, constitutes a significant factor in this context. However, the already identified risk loci can only account for around 25% of the overall heritability. Various mechanisms, including epigenetic alterations, have been suggested as potential explanations for the unexplained heritability.
Epigenetic modifications have a crucial role in governing the activation states of genes. Consequently, the disruption of any of these interdependent systems can potentially give rise to atypical gene expression, thereby contributing to the onset and progression of many diseases. Various epigenetic profiles have been documented, particularly in the context of malignancies, and more recently in many chronic inflammatory conditions.
The study of epigenetic changes is believed to import a majority of different prospectives into SpA pathophysiology, as well as the development of new diagnostic and prognostic techniques and the identification of new therapeutic agents.
The long non-coding RNA H19 (lncRNA H19) has gained significant recognition in the scientific community over the last two decades. It has been extensively utilized in a wide range of research endeavors to investigate the role of H19 in the process of genomic imprinting. Recent studies have brought attention to the pivotal role of H19 in regulating embryonic placental development and skeletal muscle differentiation.