This article discusses rheumatoid arthritis (RA) as a chronic, systemic autoimmune disease leading to progressive joint damage and multi-organ complications. The complex pathogenesis of the disease is presented, involving the interaction of environmental, genetic, and immunological factors, including the role of autoantibodies and proinflammatory cytokines. Particular attention is paid to leflunomide, a disease-modifying antirheumatic drug (DMARD), which primarily works by inhibiting the DHODH enzyme, leading to reduced T and B cell proliferation. The additional anti-inflammatory properties of the drug’s active metabolite, teriflunomide, and its impact on signaling pathways related to the immune response are also discussed. This article examines the variability in patient responses to leflunomide treatment in terms of both efficacy and toxicity, with particular emphasis on the potential role of pharmacogenetic factors. It was pointed out that polymorphisms in genes related to drug metabolism, transport, and mechanism of action may influence the pharmacokinetics and safety of the therapy. It was also emphasized that the available data are primarily derived from observational studies and small cohorts, and the results are often inconsistent. Although some genetic variants and plasma teriflunomide concentrations show potential as predictors of treatment response, the current level of evidence does not support the routine use of pharmacogenetic testing in clinical practice. The article emphasizes that the pharmacogenetics of leflunomide represents a promising, yet still exploratory, avenue of research in the context of personalized RA therapy. It emphasizes the need for larger, well-designed clinical trials and the development of standardized guidelines, which would be necessary before the potential implementation of such strategies in routine clinical practice.

Long non-coding RNAs (lncRNAs) constitute an important group of regulatory RNA molecules involved in the control of gene expression at the epigenetic, transcriptional, and post-transcriptional levels. In recent years, their crucial role in the pathophysiology of cardiovascular diseases, particularly coronary heart disease, has become increasingly evident. The aim of this review is to present current knowledge regarding the mechanisms of lncRNA action in the cardiovascular system, their involvement in the molecular processes associated with myocardial ischaemia, and their potential diagnostic and therapeutic applications. We discuss the molecular mechanisms responsible for the regulation of cardiomyocyte apoptosis, oxidative stress, mitochondrial dysfunction, angiogenesis, coronary vessel remodelling, and cardiac fibrosis. Particular attention is paid to selected lncRNAs involved in coronary heart disease, including MIAT, MALAT1, ANRIL, and H19, which influence inflammatory processes, vascular smooth muscle cell proliferation, responses to hypoxia, and cardiac fibrosis. The potential of lncRNAs as diagnostic and prognostic biomarkers in coronary artery disease is also discussed. Current evidence suggests that molecules such as MALAT1, MIAT, LIPCAR, and HCG11 may have considerable diagnostic and prognostic value, including for predicting major adverse cardiovascular events and the no-reflow phenomenon following percutaneous coronary intervention. Furthermore, contemporary therapeutic strategies targeting lncRNAs are presented, including antisense oligonucleotides, siRNAs, and CRISPR/Cas9 genome-editing technologies. Despite promising preclinical findings, the clinical application of lncRNA-based therapies remains limited by challenges related to safety, delivery of therapeutic molecules, and translation of experimental findings into clinical practice. Nevertheless, lncRNAs represent a promising avenue for the development of precision medicine and may play an important role in the future diagnosis and treatment of cardiovascular diseases.