Affecting millions of people worldwide, chronic kidney disease is a serious medical problem. It results in a decrease in glomerular filtration rate below 60 mL/min/1.73 m, albuminuria, abnormalities in urine sediment and pathologies detected by imaging studies lasting a minimum of 3 months. Patients with CKD develop uremia, and as a result of the accumulation of uremic toxins in the body, patients can be expected to suffer from a number of medical consequences such as progression of CKD with renal fibrosis, development of atherosclerosis or increased incidence of cardiovascular events. Another key element in the pathogenesis of CKD is oxidative stress, resulting from an imbalance between the production of antioxidants and the production of reactive oxygen species. Oxidative stress contributes to damage to cellular proteins, lipids and DNA and increases inflammation, perpetuating kidney dysfunction. Additionally, renal fibrogenesis involving the accumulation of fibrous tissue in the kidneys occurs. In our review, we also included examples of forms of therapy for CKD. To improve the condition of CKD patients, pharmacotherapy can be used, as described in our review. Among the drugs that improve the prognosis of patients with CKD, we can include: GLP-1 analogues, SGLT2 inhibitors, Finerenone monoclonal antibody—Canakinumab and Sacubitril/Valsartan.

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.

Insulin resistance is a condition of impaired tissue reactivity to insulin. This state is primarily associated with obesity and the lifestyle of modern Western societies, which favors abnormalities of glucose and lipid homeostasis. As a result, more and more people suffer from illnesses that develop because of the disturbed metabolic function of insulin, including type 2 diabetes, nonalcoholic fatty liver disease and polycystic ovarian syndrome. There are many studies describing the relationship between declining sensitivity to insulin and insufficient physical activity or unhealthy dietary habits. However, there is a vast number of other factors that may contribute to the development of this condition. In recent years, more attention has been paid to environmental pollutants as promoters of insulin resistance. As the overall grade of waste accumulation in the environment rises, factors like toxic metals, pesticides, dust, harmful gases and micro- or nanoplastics are starting to pose an increasingly serious threat in the context of metabolic disorder development. This review gathers data concerning the influence of the mentioned pollutants on the metabolic health of living organisms, with particular emphasis on the impact on carbohydrate processing, insulin resistance and molecular pathways associated with these processes.

IgG4-related disease (IgG4-RD) is a systemic fibroinflammatory condition characterized by the infiltration of IgG4-positive plasma cells in affected tissues, leading to fibrosis and progressive organ dysfunction. This review explores the epidemiology, pathogenesis, and organ manifestations of IgG4-RD, with a focus on autoimmune pancreatitis and sclerosing cholangitis as the main clinical presentations. It may cause exocrine and endocrine pancreatic insufficiency and chronic hepatobiliary failure. Main diagnostic challenges include differentiation from malignancies and other inflammatory conditions. Diagnosis of IgG4-RD involves combination of clinical symptoms, typical imaging findings, elevated serum IgG4 levels, and histopathological evidence of IgG4-positive plasma cell infiltration. Advances in clinical understanding of the disease, histopathological and serological markers, imaging techniques, have enhanced early detection. Current treatment strategies prioritize steroids therapy for induction of remission, while steroid-sparing agents, including disease-modifying antirheumatic drugs and rituximab play the pivotal roles in managing its relapses or steroid-resistant disease. Biologic therapies are also promising therapeutic avenues. In addition, multidisciplinary approach optimizes the diagnosis, treatment, and long-term outcomes in this complex disease.

Myocardial infarction (MI) among athletes is an uncommon but clinically significant event that has attracted growing attention because of its potential to cause sudden cardiac death (SCD) and long-term morbidity in an otherwise healthy population. This review synthesizes current literature on the epidemiology, pathophysiology, diagnostic evaluation, and preventive strategies for MI in athletes across age groups. In athletes younger than approximately 35 years, MI is rare and is more often attributable to non-atherosclerotic mechanisms—congenital coronary artery anomalies, spontaneous coronary artery dissection, coronary artery spasm, myocardial bridging, an oxygen supply–demand mismatch related to hypertrophic cardiomyopathy, or performance-enhancing substance use—than to classic atherosclerotic coronary artery disease. In masters athletes, generally older than 35 years, atherosclerotic plaque rupture or erosion, frequently triggered by the acute hemodynamic stress of intense exertion, becomes the predominant mechanism. Preparticipation cardiovascular screening, incorporating structured history-taking, physical examination, and standardized electrocardiographic interpretation criteria, together with the widespread availability of automated external defibrillators and bystander cardiopulmonary resuscitation training, constitutes the principal preventive strategy, although its optimal design and cost-effectiveness remain debated. Following an acute event, individualized, shared-decision-making approaches to return-to-play balance the cardiovascular and psychological benefits of continued exercise against residual arrhythmic and ischemic risk. Continued research into advanced imaging biomarkers, genetic testing, and risk-stratification tools is needed to refine clinical care for this distinctive population.

Autophagy is a key lysosome-dependent degradation pathway essential for maintaining cellular homeostasis, particularly in the highly secretory pancreas. This review summarizes recent advances in autophagy, selective autophagy, and vesicle trafficking in pancreatic physiology and disease. We focus on the dual role of autophagy, which can support cellular protection and organelle quality control, but also contribute to pathology when dysregulated. We highlight emerging molecular mechanisms linking autophagy with vesicle trafficking systems, including membrane remodeling, organelle contact sites, and key regulators such as VMP1 and Beclin-1. In addition, we discuss the role of autophagy in pancreatic inflammation and cancer, emphasizing its context-dependent function. Finally, we outline recent translational approaches targeting autophagy-related pathways, including pharmacological and genetic strategies, with potential diagnostic and therapeutic relevance in pancreatic diseases.