Cardiovascular aging is a multifactorial and systemic process that contributes significantly to the global burden of cardiovascular disease, particularly in older populations. This review explores the molecular and cellular mechanisms underlying cardiovascular remodeling in age-related conditions such as hypertension, atrial fibrillation, atherosclerosis, and heart failure. Central to this process are chronic low-grade inflammation (inflammaging), oxidative stress, cellular senescence, and maladaptive extracellular matrix remodeling. These hallmarks of aging interact to impair endothelial function, promote fibrosis, and compromise cardiac and vascular integrity. Key molecular pathways—including the renin–angiotensin–aldosterone system, NF-κB, NLRP3 inflammasome, IL-6, and TGF-β signaling—contribute to the transdifferentiation of vascular cells, immune dysregulation, and progressive tissue stiffening. We also highlight the role of the senescence-associated secretory phenotype and mitochondrial dysfunction in perpetuating inflammatory and fibrotic cascades. Emerging molecular therapies offer promising strategies to reverse or halt maladaptive remodeling. These include senescence-targeting agents (senolytics), Nrf2 activators, RNA-based drugs, and ECM-modulating compounds such as MMP inhibitors. Additionally, statins and anti-inflammatory biologics (e.g., IL-1β inhibitors) exhibit pleiotropic effects that extend beyond traditional risk factor control. Understanding the molecular basis of remodeling is essential for guiding future research and improving outcomes in older adults at risk of CVD.

Vitamin D, long recognized for its essential role in calcium–phosphate balance and bone health, has increasingly been identified as a pleiotropic regulator of metabolic, cardiovascular, and renal function. Deficiency of vitamin D is widespread worldwide and has been linked to a higher risk of insulin resistance, type 2 diabetes, atherosclerosis, hypertension, and chronic kidney disease. Meta-analyses suggest that each 10 nmol/L (≈4 ng/mL) increase in serum 25-hydroxyvitamin D [25(OH)D] is associated with about a 4% lower risk of type 2 diabetes, whereas other analyses indicate an approximately 10% reduction in cardiovascular event risk per 10 ng/mL (≈25 nmol/L) increment in circulating 25(OH)D concentration. Clinical and epidemiological studies suggest that optimal 25(OH)D concentrations may protect against cardiometabolic and renal complications, though supplementation trials show heterogeneous outcomes depending on baseline vitamin D status, genetic background, and dosage. By synthesizing current knowledge, this work highlights vitamin D status as a potentially modifiable determinant of global disease burden and a target for preventive and therapeutic strategies.

Oxidative stress, caused by an imbalance between the production of reactive oxygen species and endogenous antioxidant capacity, is a key etiological factor in numerous pathologies, including neurodegenerative and cardiovascular diseases. The limited clinical efficacy of conventional antioxidants is primarily due to their insufficient accumulation within the mitochondria, the main site of intracellular ROS generation. This article reviews the design and application of Mitochondria-Targeted Antioxidants, which represent a major advance in precision medicine. The design of these compounds involves linking an antioxidant “payload” to a lipophilic cation, such as the triphenylphosphonium group. This positive charge leverages the negative electrochemical gradient across the inner mitochondrial membrane to drive the antioxidant into the organelle. This mechanism allows the drug to reach concentrations over 100 times higher than non-targeted alternatives. The discussion encompasses the structure-activity analysis of the carrier, the payload (e.g., quinone derivatives), and the linker, which determine optimal subcellular partitioning and scavenging efficiency. Preclinical data highlight the therapeutic potential of this approach, showing strong neuroprotection in models of Parkinson’s and Alzheimer’s diseases, as well as improved outcomes in cardiovascular and ocular health. By restoring redox balance specifically within the mitochondria, these targeted therapies offer a more effective way to treat chronic oxidative damage.

Acute kidney injury (AKI), chronic kidney disease (CKD), and diabetic kidney disease (DKD) are interconnected disorders linked by shared mechanisms involving redox imbalance and mitochondrial dysfunction. This review summarizes current evidence on the role of excessive reactive oxygen species (ROS) production, impaired oxidized nicotinamide adenine dinucleotide (NAD⁺) metabolism, altered mitochondrial bioenergetics, disrupted mitochondrial dynamics, and defective mitochondrial quality control pathways, including mitophagy and the mitochondrial unfolded protein response (UPR^mt), in kidney disease progression. Experimental and clinical studies indicate that these mechanisms contribute to inflammation, fibrosis, apoptosis, and maladaptive repair, promoting progression from AKI to CKD and worsening DKD. The review also discusses emerging biomarkers and therapeutic strategies targeting oxidative stress and mitochondrial dysfunction. Overall, redox-mediated mitochondrial injury represents a shared pathogenic axis and a potential therapeutic target across kidney diseases.

The coronavirus disease 2019 (COVID-19) pandemic has revealed a close and multifaceted relationship between viral infection, systemic inflammation, and cardiovascular health. Among the cardiac complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), atrial fibrillation (AF)—especially new-onset atrial fibrillation (NOAF)—has emerged as a major determinant of disease severity and prognosis. Clinical studies and meta-analyses show that 5–10% of hospitalized COVID-19 patients develop AF, with markedly higher rates in critically ill individuals. Both pre-existing and NOAF are independently associated with increased risks of intensive care admission, mechanical ventilation, thromboembolic events, and mortality. The underlying mechanisms involve a combination of cytokine-mediated inflammation, endothelial dysfunction, microvascular injury, and dysregulation of the renin–angiotensin–aldosterone system (RAAS). Viral downregulation of angiotensin-converting enzyme 2 (ACE2) receptors contributes to myocardial fibrosis, while hypoxia, oxidative stress, and autonomic imbalance further promote electrical remodeling and arrhythmogenesis. Post-infectious studies indicate that atrial structural changes and autonomic dysfunction may persist for months, predisposing survivors to recurrent arrhythmias. Technological advances in telecardiology and digital medicine have provided new tools for early detection and long-term monitoring. Wearable electroencephalography (ECG) devices, implantable loop recorders (ILRs), and artificial intelligence (AI)-based diagnostic algorithms enable continuous rhythm surveillance and individualized management, improving outcomes in post-COVID patients. This review summarizes current evidence on the epidemiology, pathophysiology, clinical implications, and monitoring strategies of AF in COVID-19. It underscores the importance of integrating telemedicine and AI-assisted diagnostics into cardiovascular care to mitigate the long-term arrhythmic and systemic consequences of SARS-CoV-2 infection.

Liquid biopsy has emerged as one of the most promising approaches in precision oncology by enabling minimally invasive, real-time molecular characterization of tumors. Despite growing evidence, its clinical utility in urogenital cancers remains insufficiently defined. Differences in tumor biology, assay sensitivity and availability of tumor-derived material limit the assessment of its diagnostic, prognostic and predictive value across individual malignancies. This review summarizes the biological basis of liquid biopsy and evaluates its current and emerging clinical applications in prostate, bladder, renal cell, testicular, and penile cancers. Particular emphasis is placed on its potential for molecular tumor characterization, risk stratification, treatment selection, monitoring of therapeutic response and resistance, and detection of minimal residual disease. The current evidence indicates that liquid biopsy provides complementary information to tissue biopsy, particularly by enabling repeated sampling and longitudinal monitoring of tumor evolution. Its clinical value appears most relevant when tissue acquisition is challenging or dynamic molecular assessment is required. However, important limitations include low levels of tumor-derived material in selected malignancies, methodological heterogeneity, and insufficient prospective validation. Liquid biopsy should currently be considered a complementary rather than a replacement approach to tissue biopsy. Further technological advances, methodological standardization, and prospective clinical validation may facilitate its broader integration into clinical practice and support more precise diagnosis, treatment monitoring, and personalized management of urogenital cancers.