Biomarkers play a crucial role in various stages of disease management, including screening, diagnosis, prediction, prognosis, treatment, and safety monitoring. Although they are powerful tools in disease diagnosis, management, and drug development, identifying and validating reliable biomarkers remains a significant challenge. Among potential microbiome-derived biomarkers, trimethylamine N-oxide (TMAO) has gained notable attention for its link to atherosclerosis and cardiovascular risk. However, despite the growing body of research on TMAO, its practical application in clinical settings for disease management and patient outcome enhancement is still not a reality. This paper presents recent data on the utility of TMAO as a cardiovascular biomarker, categorized by its various roles: diagnostic, prognostic, susceptibility/risk, monitoring, pharmacodynamic/response, predictive, and safety. It also briefly discusses research on TMAO’s potential role in cardiovascular disease development. While TMAO shows promise, particularly in prognostic applications, its reliability as a biomarker has been inconsistent across studies. These variances may result from several confounding factors that affect TMAO plasma levels, including diet, kidney function, and demographic variables. The review aims to elucidate the specific contexts in which TMAO can be valuable, potentially leading to more personalized and effective management of cardiovascular disease.

Evidence suggests that microbiota-derived metabolites, including short-chain fatty acids (SCFAs) and trimethylamine-oxide (TMAO), affect the course of diabetic multiorgan pathology. We hypothesized that diabetes activates the intestinal renin–angiotensin system (RAS), contributing to gut pathology. Twelve-week-old male rats were divided into three groups: controls, diabetic (streptozotocin-induced) and diabetic treated with enalapril. Histological examination and RT-qPCR were performed to evaluate morphology and RAS expression in the jejunum and the colon. SCFA and TMAO concentrations in stools, portal and systemic blood were evaluated. In comparison to the controls, the diabetic rats showed hyperplastic changes in jejunal and colonic mucosa, increased plasma SCFA, and slightly increased plasma TMAO. The size of the changes was smaller in enalapril-treated rats. Diabetic rats had a lower expression of Mas receptor (MasR) and angiotensinogen in the jejunum whereas, in the colon, the expression of MasR and renin was greater in diabetic rats. Enalapril-treated rats had a lower expression of MasR in the colon. The expression of AT1a, AT1b, and AT2 receptors was similar between groups. In conclusion, diabetes produces morphological changes in the intestines, increases plasma SCFA, and alters the expression of renin and MasR. These alterations were reduced in enalapril-treated rats. Future studies need to evaluate the clinical significance of intestinal pathology in diabetes.

Diuretics are essential for managing fluid overload in heart failure (HF) and controlling blood pressure in hypertension. However, their use is often associated with complications such as electrolyte imbalances and neurohormonal dysregulation, which can limit their effectiveness and contribute to adverse outcomes. These challenges underscore the need for alternative or adjunctive strategies to better manage fluid retention and congestion. Osmolytes are small molecules that help counteract increases in extracellular osmotic and hydrostatic pressure and are naturally present at high concentrations in the renal medulla. Notably, elevated serum levels of osmolytes such as trimethylamine N-oxide (TMAO) and betaine have been observed in patients with HF, although their role in the pathophysiology of the disease remains unclear. Given the known diuretic properties of osmolytes such as urea—historically used in the management of HF—it is plausible that other osmolytes may similarly modulate diuresis and volume status. This review examines the biological actions of several key osmolytes, including urea, TMAO, betaine, and taurine. Emerging evidence supports the need for further preclinical and clinical studies to investigate the potential diuretic and cytoprotective effects of TMAO, betaine, and taurine in the prevention and treatment of HF and hypertension.

Introduction Heart rate variability (HRV) serves as a non-invasive marker to assess autonomic nervous system (ANS) modulation on cardiac rhythm. Its link with sleep quality, particularly in the context of insomnia, posits HRV as a potential indicator of autonomic state variations during sleep disturbances. The prevalence of insomnia, affecting up to 20% of the general population, emphasizes the need to understand its extensive impact. Material and Methods For this review - 41 relevant titles from 1985 to 2024 were selected Analysis of the Literature: Recent studies highlight a bidirectional relationship between insomnia and ANS function, with increased sympathetic activity indicated by physiological and subjective measures in individuals with insomnia. The role of medications like beta-blockers in disrupting ANS and leading to sleep deprivation further connects measurable and perceived aspects of sleep quality, impacting health negatively. Moreover, HRV's application has expanded beyond professional athletics to daily activity and sleep quality monitoring by the general population, emphasizing its potential in evaluating stress and training intensity. Conclusion: The complex interplay between HRV, insomnia, and health outcomes necessitates further research. However, integrating HRV measurements into clinical and everyday monitoring may offer a promising avenue for improving sleep disorder management and enhancing quality of life.

This narrative review examines current and emerging treatment strategies for diabetic macular edema (DME), a complication of diabetic retinopathy characterised by fluid accumulation in the macula, which can lead to vision impairment. The incidence of DME is particularly high in patients with long-standing diabetes and advanced retinopathy. The current treatment options for DME include anti-vascular endothelial growth factor (anti-VEGF) agents, corticosteroids, and laser therapies. Anti-VEGF agents, including bevacizumab, ranibizumab, aflibercept, and the more recently developed brolucizumab and faricimab, have been demonstrated to reduce macular thickness and improve visual acuity. Brolucizumab offers the advantage of fewer injections due to its longer duration of action, although it carries a higher risk of ocular inflammation compared to other anti-VEGF agents. The dual inhibition of the VEGF and angiopoietin-2 (Ang-2) pathways by faricimab may enhance vascular stability and reduce inflammation, potentially improving patient outcomes. Steroid therapies, including dexamethasone, fluocinolone acetonide, and triamcinolone acetonide, represent an alternative for patients who do not respond adequately to anti-VEGF treatment. Laser therapies, including focal, navigated, and subthreshold laser treatments, remain a crucial component in the management of DME, with the ability to seal leaking vessels and reduce fluid accumulation. In order to achieve the best outcomes for patients, it is essential to continue to advance these treatment modalities and adopt a personalised, multifaceted approach.

Introduction and purposeAndrogenetic alopecia (AGA) is one of the most common causes of baldness worldwide. It affects up to 80% of men by the age of 70 and up to 40% of postmenopausal women. In AGA etiology and pathogenesis, the three essential components play a key role - genetic inheritance, patient age and hormonal effects of androgens. In the following review, we have described the available FDA-approved and off-label treatments for AGA, along with their efficacy and potential side effects that should always be considered to prevent treatment discontinuation by the patients.The state of knowledgeThe pathogenesis of AGA is based on inherited dihydrotestosterone (DHT) sensitivity in the scalp skin, which leads to progressive hair loss. The literature documents the effectiveness of several treatments with different mechanisms of action in AGA therapy, but only topical minoxidil and oral finasteride gained FDA approval so far. Minoxidil acts by the blood vessels dilatation that increases the flow of oxygenated and growth factor-enriched blood to the hair follicles in the skin. 5-alpha reductase inhibitors, such as finasteride and dutasteride are another threapeutic option. Thy act by the inhibition of 5-alpha reductase, the enzyme which converts testosterone to DHT - the main causative agent of androgenetic alopecia. Recently, topical applications of minoxidil and finasterid, along with completely new emerging treatments for androgenetic alopecia are gaining popularity among doctors and patients. SummaryThis review describes current treatments for AGA, considering their efficacy, optimal doses, and the most common side effects. An important fact to emphasise is that androgenetic alopecia is based on a genetic predisposition, and treatment requires long-term use. For this reason, when choosing a medication, it is essential to cooperate with the patient and combine different therapeutic methods to achieve the desirable outcome while avoiding adverse reactions.