Calcific aortic valve disease (CAVD) is a multifactorial condition. Both environmental and genetic factors play an important role in its etiology. CAVD exhibits a broad spectrum, varying from mild valve thickening to severe valve calcification and stenosis. Progression of the disease consists of chronic inflammation, lipoprotein deposition, and active leaflet calcification. It is a process similar to coronary artery disease. In this study, we investigated Lp(a) levels and gene polymorphisms associated with calcific aortic stenosis from blood samples after echocardiography in the evaluation of 75 patients diagnosed with CAVD and 77 controls. Blood tests were run in our laboratory to rule out certain risk factors before echocardiography examination. A significant association among smoking, elevated LDL level and creatinine, low albumin levels, Lp(a) level, rs10455872, and rs3798220 polymorphisms may be considered genetic risk factors for the development of calcific aortic stenosis.

This comprehensive review explores the critical roles of microRNAs (miRNAS) in cardiovascular diseases, emphasizing their regulatory functions in gene expression and their involvement in disease progression. miRNAS are small, evolutionarily conserved non-coding RNAs that regulate gene expression post-transcriptionally and play essential roles in various cardiac conditions, including fibrosis, cardiac remodeling, apoptosis, ischemia/reperfusion injury, hypertrophy, heart failure, arrhythmias, coronary artery disease (CAD), congenital heart diseases (CHDs), cardiomyopathies, and valvular heart disease (VHD). miRNAS are increasingly recognized as sensitive and specific biomarkers for early diagnosis, disease monitoring, and evaluation of therapeutic responses across the cardiovascular disease spectrum. Ischemia/reperfusion injury leads to significant cardiac damage through elevated oxidative stress, mitochondrial dysfunction, and apoptosis. CAD, a major contributor to global morbidity and mortality, is primarily driven by atherosclerosis and chronic inflammation. Cardiac hypertrophy is initially an adaptive response to stress but may progress to heart failure if sustained. Arrhythmias arise from electrical disturbances such as reentry, abnormal automaticity, and triggered activity. Heart failure is a complex and progressive syndrome marked by poor prognosis and increasing global prevalence. VHD involves intricate molecular alterations, including myocardial fibrosis and calcification, which contribute to disease progression and adverse outcomes. Cardiomyopathies—including hypertrophic, dilated, restrictive, and arrhythmogenic forms—are influenced by genetic mutations, systemic diseases, and disrupted molecular signaling. CHDs, the most common congenital malformations, stem from structural abnormalities in cardiac development and remain a major cause of infant morbidity and mortality. Novel therapeutic methods, such as antisense oligonucleotides, miR mimics, and exosome-based delivery mechanisms, demonstrate the translational promise of miRNAs in the realm of personalized cardiovascular medicine. However, issues such as small sample sizes, inconsistent results, interspecies differences, and delivery challenges restrict the clinical application of miRNA-based therapies. This review integrates mechanistic insights, critiques the quality of available evidence, and identifies translational shortcomings. It highlights the diagnostic, prognostic, and therapeutic potential of miRNAs in reshaping cardiovascular disease treatment.

Heart diseases (HDs) continue to be among the major diseases that adversely affect human health worldwide, with complex interactions between genetic, environmental, and biochemical factors contributing to their progression. These include coronary heart disease, hypertension, heart failure, vascular calcification, etc. Cardiovascular diseases have been extensively studied in the Framingham Heart Study since 1948, spanning three generations over the past 70 years, and are highly correlated with various factors, including biochemical, environmental, behavioral, and genetic factors. In recent years, epigenetic mechanisms have emerged as crucial regulators of cardiovascular pathology, influencing gene expression without altering the underlying DNA sequence. Moreover, early detection and diagnosis of heart diseases are crucial for improving treatment and prognosis. Recent studies on heart disease have found that the expression of potential candidate genes related to the disease is associated with epigenetic mechanisms. Indeed, abnormal methylation states have been detected in candidate genes that can serve as biomarkers to assess the progression of heart disease. Recent advances in next-generation sequencing techniques have contributed significantly to our understanding of heart diseases, including the role of DNA methylation, adenosine triphosphate (ATP)-dependent chromatin conformation and remodeling, post-translational modifications of histones and non-coding RNAs. Lastly, this review examines the latest discoveries in the epigenetic regulation of heart diseases, highlighting the roles of DNA methyltransferases (DNMTs), histone deacetylases (HDACs), sirtuins (SIRTs), and ten-eleven translocation proteins (TETs). Additionally, this review highlights preclinical therapeutic strategies targeting epigenetic modifiers, offering new avenues for precision medicine in cardiology. Understanding these epigenetic pathways is crucial for developing novel biomarkers and epigenetic-based therapies that aim to reverse maladaptive cardiac remodeling and enhance clinical outcomes.

Survivin is a bifunctional protein which regulates cell division and inhibits apoptosis. Survivin is a member of the inhibitor of apoptosis protein (IAP) family. Expression of survivin has been shown to be responsible for apoptosis and resistance to ionizing radiation. The aim of the present study was to investigate the association between −31 G/C promoter polymorphism, survivin protein and glial tumour grading, and to compare survivin versus Ki-67 as a marker. In this study, DNA was isolated from paraffin-embedded sections of 29 patients diagnosed with glial tumours. Survivin gene promoter −31 G/C polymorphism was investigated using PCR-RFLP. For the analysis, 10 µm sections were stained with survivin protein and Ki-67 antibody. Immunohistochemical staining was performed. Survivin showed a positive correlation with Ki-67 (r = 0.604; p = 0.001). The tumour grades correlated with survivin; however, the relationship was not statistically significant (r = 0.345; p > 0.05). We found a significant correlation between tumour grades and Ki-67 (r = 0.663; p < 0.01), suggesting that Ki-67 is a more sensitive marker compared to survivin.

Alteration of methylation is a process seen across a wide variety of species ranging from bacterial microorganisms to mammals, defined as the adaptation method the organism develops against environmental or intrinsic effects, or employs to switch off the genome regions which are no longer required through the evolutionary process. Scientific advancements have allowed detecting the regions that undergo different patterns of methylation. It has been demonstrated that the control on changes in gene expression is not guided by transcription factors alone and that epigenetic alterations are also involved in this process. Furthermore, epigenetic modifications have been shown to be considerably important in cancer development. This section focuses on epigenetic changes and potential treatment options in lung cancer.