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.

Mutation detection in the promoter region of survivin gene on N-methyl-N-nitrosourea induced colon tumor model in experiment

There are two types of radiation, namely ionising and non-ionising radiation, the former of which interacts with atoms or molecules while the latter does not. Technological advances, evolving with the development of mankind, have led to gradually increasing exposure to radiation. Radiation-related influences affect the cells that make up organisms in different ways, which means that they result in various effects in the affected organism. DNA methylation altered by radiation is one of the cellular systems affected in this context. DNA methylation is a major epigenetic mechanism that is particularly associated with cellular radiosensitivity, and it may also be associated with increased resistance to radiotherapy or chemotherapy. There is increasing scientific evidence that support this notion across a variety of study types from those that involve plants to those conducted with human subjects. Recent results with an increasing trend are available in this field. Our aim in this chapter is to describe the radiation environment and increasing exposure among humans as well as other living species, and to shed light on the effects of radiation on epigenetic mechanisms based on relevant scientific studies.

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.