Hypertension stands as a pervasive global health challenge, contributing significantly to mortality rates worldwide. Various factors, including lifestyle choices and dietary habits, contribute to the development of hypertension. In recent years, oxidative stress has garnered significant attention as a factor influencing hypertension risk, prompting a shift in research focus towards exploring it as a potential target for prevention and treatment. Antioxidants found in our diet, such as vitamins C, E and carotenoids exhibit the ability to neutralize reactive oxygen species, thereby mitigating oxidative stress. In addition, Vitamin A has an antioxidant effect despite not being an antioxidant itself. Consequently, supplementation or increased intake of these antioxidants has been hypothesized to potentially lower blood pressure levels and aid in the management of hypertension, thereby potentially prolonging life expectancy. Research findings regarding this effect have been diverse. This paper examines the existing literature demonstrating favorable outcomes associated with antioxidant supplementation.

Cardiovascular diseases stand as the predominant global cause of mortality, exerting a profound impact on both life expectancy and its quality. Given their immense public health burden, extensive efforts have been dedicated to comprehending the underlying mechanisms and developing strategies for prevention and treatment. Selenium, a crucial participant in redox reactions, emerges as a notable factor in maintaining myocardial cell homeostasis and influencing the progression of cardiovascular disorders. Some disorders, such as Keshan disease, are directly linked with its environmental deficiency. Nevertheless, the precise extent of its impact on the cardiovascular system remains unclear, marked by contradictory findings in the existing literature. High selenium levels have been associated with an increased risk of developing hypertension, while lower concentrations have been linked to heart failure and atrial fibrillation. Although some trials have shown its potential effectiveness in specific groups of patients, large cohort supplementation attempts have generally yielded unsatisfactory outcomes. Consequently, there persists a significant need for further research aimed at delineating specific patient cohorts and groups of diseases that would benefit from selenium supplementation.

Inflammation has been widely recognized as one of the major pathophysiological drivers of the development of atrial fibrillation (AF), which works in tandem with other risk factors of AF including obesity, diabetes, hypertension, and heart failure (HF). Our current understanding of the role of inflammation in the natural history of AF remains elusive; however, several key players, including the NLRP3 (NLR family pyrin domain containing 3) inflammasome, have been acknowledged to be heavily influential on chronic inflammation in the atrial myocardium, which leads to fibrosis and eventual degradation of its electrical function. Nevertheless, our current methods of pharmacological modalities with reported immunomodulatory properties, including well-established classes of drugs e.g., drugs targeting the renin–angiotensin–aldosterone system (RAAS), statins, and vitamin D, have proven effective in reducing the overall risk of developing AF, the onset of postoperative atrial fibrillation (POAF), and reducing overall mortality among patients with AF. This might bring hope for further progress in developing new treatment modalities targeting cellular checkpoints of the NLRP3 inflammasome pathway, or revisiting other well-known anti-inflammatory drugs e.g., colchicine, vitamin C, nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticosteroids, and antimalarial drugs. In our review, we aim to find relevant upstream anti-inflammatory treatment methods for the management of AF and present the most current real-world evidence of their clinical utility.

Systemic sclerosis (SSc) represents a rare and intricate autoimmune connective tissue disease, the pathophysiology of which has not been fully understood. Its key features include progressive fibrosis of the skin and internal organs, vasculopathy and aberrant immune activation. While various anti-nuclear antibodies can serve as biomarkers for the classification and prognosis of SSc, their direct role in organ dysfunction remains unclear. Anti-Th/To antibodies are present in approximately 5% of SSc patients, and are particularly prevalent among those with the limited subtype of the disease. Although the presence of these autoantibodies is associated with a mild course of the disease, there is a strong connection between them and severe clinical manifestations of SSc, including interstitial lung disease, pulmonary arterial hypertension and gastrointestinal involvement. Also, the additional clinical correlations, particularly with malignancies, need further research. Moreover, the disease’s course seems to be influenced by antibodies, specific serum cytokines and TLR signaling pathways. Understanding the relationships between presence of anti-Th/To, its molecular aspects and response to treatment options is crucial for the development of novel, personalized therapeutic techniques and should undergo profound analysis in future studies.

In lung cancer patients, two complementary abnormalities were found that can cause disruption of the mitochondrial network: increased fusion and impaired fission, manifested by reduced levels of FIS1, a mitochondrial division regulator, and increased expression of MFN1, a mitochondrial fusion mediator. Immunoexpression studies of MFN1 and FIS1 proteins were performed in serum samples obtained from 47 patients with non-small cell lung cancer (NSCLC) and 21 controls. In the NSCLC patients, the immunoexpression of the MFN1 protein was significantly higher, and the FIS1 protein level was significantly lower than in the control group (p < 0.01; p < 0.001; UMW test). Patients with early, operable lung cancer had significantly lower levels of MFN1 immunoexpression compared to patients with advanced, metastatic lung cancer (p < 0.05; UMW test). This suggests that early stages of the disease are characterized by greater fragmentation of damaged mitochondria and apoptosis. In contrast, lower FIS1 protein levels were associated with a worse prognosis. Increased mitochondrial fusion in the blood of lung cancer patients may suggest an increase in protective and repair mechanisms. This opens up questions about why these mechanisms fail in the context of existing advanced cancer disease and is a starting point for further research into why protective mechanisms fail in lung cancer patients.

Mitral valve prolapse (MVP) is a relatively common mitral valvulopathy and the most common cause of isolated primary mitral regurgitation (MR) requiring surgical repair. It affects about 1–3% of t