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Diabetes is a common chronic disease. Untreated diabetes may lead to complications such as nephropathy, neuropathy, retinopathy, and macroangiopathies. The main goal in treating diabetes is to limit the development of vascular complications. The FGF (fibroblast growth factor) family, with its potential as a biomarker for diabetic complications, offers a promising avenue for future research and treatment. The study aimed to analyze and compare the concentrations of selected fibroblast growth factors, FGF-2, FGF-19, FGF-22, and FGF-23, in the plasma of patients with type 1 and type 2 diabetes with those of the control group. The study group consisted of 73 patients, including 33 people with type 1 diabetes (18 M and 15 W) aged 18 to 68 years and 40 with type 2 diabetes (20 M and 20 W) aged 25 to 90. The control group consisted of 41 healthy individuals (23 men and 18 women) aged 21 to 56. The FGF-2, FGF-19, FGF-22, and FGF-23 concentrations were measured using ELISA. The study observed a significant relationship between the levels of FGF19 and FGF22 in the serum of patients with type 1 and type 2 diabetes, as well as in the control group (p < 0.001; p < 0.001). Statistical analysis revealed a significant relationship between FGF-2 and FGF-22 concentrations and hypertension (p = 0.03; p = 0.01). A statistically significant difference was also found between the concentrations of FGF-19 and FGF-22 (p = 0.001; p < 0.001) in the serum of people with normal weight and people with overweight and obesity. A significant correlation was also observed between the concentrations of FGF-22 and FGF-23 and arthritis (p = 0.01; p = 0.02). FGF-2, FGF-19, FGF-22, and FGF-23 likely significantly impact diabetes and its complications. In the future, they could serve as biomarkers for diabetic complications, aiding in diagnosis, patient monitoring, and even predicting potential complications for individuals. However, more research in this area is necessary.

Transforming growth factor-β (TGF-β) is a key protein family member that includes activins, inhibins, and bone morphogenetic proteins (BMPs). It is essential in numerous biological processes, such as chemotaxis, apoptosis, differentiation, growth, and cell migration. TGF-β receptors initiate signaling through two primary pathways: the canonical pathway involving Smad proteins and non-canonical pathways that utilize alternative signaling mechanisms. When TGF-β signaling is disrupted, it has been shown to contribute to the development of various diseases, including cancer. Initially, TGF-β effectively inhibits the cell cycle and promotes apoptosis. However, its role can transition to facilitating tumor growth and metastasis as the disease progresses. Moreover, TGF-β drives cancer progression through epithelial–mesenchymal transition (EMT), modulation of factor expression, and evasion of immune responses. This complexity establishes the need for further research, particularly into pharmacological agents targeting TGF-β, which are emerging as promising therapeutic options. Current clinical and preclinical studies are making significant strides toward mitigating the adverse effects of TGF-β. This underscores the critical importance of understanding its underlying mechanisms to enhance treatment effectiveness and improve survival rates for cancer patients.

Diabetes mellitus (DM) is a common global metabolic disease. Oxidative stress from reactive oxygen species (ROS) contributes to its development and leads to complications like heart disease, kidney failure, and stroke. Chronic inflammation in diabetes is associated with insulin resistance and elevated glucose levels, as indicated by increased markers of interleukin-6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor-alpha (TNF-α). This study investigates the activity and concentration of antioxidant enzymes (SOD, GPX1, CAT) and inflammatory markers (IL-6, CRP, TNF-α) in patients with type 1 and type 2 diabetes compared to healthy controls. The study included 73 patients—33 with type 1 diabetes (18 men, 15 women) and 40 with type 2 diabetes (20 men, 20 women)—and 41 healthy controls (23 men, 18 women). Antioxidant enzymes and inflammatory markers were measured using enzyme-linked immunosorbent assay (ELISA), and HbA1c levels were assessed. Program R and Statistica 13 were used to analyze the results. Group membership had a significant impact on SOD and CAT activity ( p  < 0.0001) and GPX1 ( p  < 0.001). BMI correlated with CAT concentration ( p  < 0.0001). SOD activity was affected by comorbidities, such as arthritis and urinary tract issues ( p  = 0.03). Diabetes markedly altered inflammatory markers, particularly CRP and TNF-α ( p  < 0.0001), and higher IL-6 levels were found in patients using medications other than metformin ( p  = 0.01). Type 1 and 2 diabetes significantly affect antioxidant enzyme activity and concentration. High SOD and GPX activity suggests chronic oxidative stress, while increased BMI is linked to lower enzyme levels. Additionally, TNF-α levels rise with diabetes duration, which may serve as a biomarker for disease progression and complications, potentially helping to predict diabetic complications and insulin resistance.

Long-term survival after solid organ transplantation remains limited by chronic remodeling, fibrosis, vascular complications, and malignancy despite advances in immunosuppressive therapy. Current monitoring strategies primarily rely on functional and immunological parameters that often identify complications only after irreversible injury has occurred. There is a critical need for earlier, mechanistically informative biomarkers that can predict survival outcomes. Many platelet-associated growth factors (PDGF, TGF-β, VEGF, EGF, and IGF-1) are stored in platelet α-granules but can also originate from immune, endothelial, and stromal cells, regulate angiogenesis, extracellular matrix deposition, immune modulation, and tissue repair—processes central to graft adaptation and chronic injury. In this review, we propose the growth factor signaling network as a conceptual framework that potentially links platelet biology, ischemia-reperfusion injury, alloimmune responses, and chronic immunosuppression to sustained growth factor signaling and maladaptive graft remodeling. This framework should be interpreted as a biologically plausible integrative model rather than a fully validated mechanistic pathway in transplant recipients. Importantly, direct clinical evidence linking platelet activation markers (e.g., P-selectin, PF4, β-thromboglobulin) with circulating growth factor levels and long-term transplant outcomes remains limited, highlighting a critical gap in current biomarker research. Emerging clinical evidence suggests their potential prognostic relevance in transplant outcomes. Elevated TGF-β levels have been associated with increased risk of opportunistic infections, while early postoperative IGF-1 concentrations predict short-term survival. Increased VEGF-A levels correlate with primary graft dysfunction and cardiac allograft vasculopathy, while PDGF isoforms contribute to fibrotic and vascular progression across transplanted organs. However, their clinical applicability is limited by methodological variability and lack of large-scale validation. Rather than serving solely as markers of rejection, platelet-associated growth factors may reflect dynamic processes involved in transplant remodeling and mortality risk. Incorporating growth factor profiling into multiparametric survival prediction models may improve early risk stratification and support precision post-transplant management strategies.

Malignant tumors are the second most common cause of death worldwide. More attention is being paid to the link between the body’s impaired oxidoreductive balance and cancer incidence. Much attention is being paid to polyphenols derived from plants, as one of their properties is an antioxidant character: the ability to eliminate reactive oxygen and nitrogen species, chelate specific metal ions, modulate signaling pathways affecting inflammation, and raise the level and activity of antioxidant enzymes while lowering those with oxidative effects. The following three compounds, resveratrol, quercetin, and curcumin, are polyphenols modulating multiple molecular targets, or increasing pro-apoptotic protein expression levels and decreasing anti-apoptotic protein expression levels. Experiments conducted in vitro and in vivo on animals and humans suggest using them as chemopreventive agents based on antioxidant properties. The advantage of these natural polyphenols is low toxicity and weak adverse effects at higher doses. However, the compounds discussed are characterized by low bioavailability and solubility, which may make achieving the blood concentrations needed for the desired effect challenging. The solution may lie in derivatives of naturally occurring polyphenols subjected to structural modifications that enhance their beneficial effects or work on implementing new ways of delivering antioxidants that improve their solubility and bioavailability.

Melatonin, a key regulator of the circadian rhythm, exerts strong antioxidant effects by scavenging reactive oxygen species (ROS) and modulating enzymatic redox balance. Xanthine oxidoreductase (XOR), a molybdenum- and iron–sulfur-containing enzyme, catalyzes the oxidation of hypoxanthine to xanthine and xanthine to uric acid—the final steps of purine catabolism—serving as an important enzymatic source of ROS under physiological conditions. XOR exists in three interconvertible isoforms: xanthine dehydrogenase (XDH), which uses NAD+ as an electron acceptor; xanthine oxidase (XO), which transfers electrons to oxygen, producing superoxide and hydrogen peroxide; and an intermediate form (XDO) that reflects the redox-dependent interconversion between the two. This study aimed to evaluate temporal and sex-dependent variations in XOR isoforms and their relationship with melatonin levels in healthy individuals. Sixty-six volunteers (33 women aged 24–38 and 33 men aged 24–44) were examined. Blood samples were collected at 02:00, 08:00, 14:00, and 20:00. Serum melatonin was measured using ELISA, and XOR isoform activities were determined spectrophotometrically. Melatonin exhibited a precise 24 h rhythm with a nocturnal peak at 02:00 (~98 pg/mL) and a daytime nadir at 14:00 (~9 pg/mL). XO activity varied significantly (p < 0.01), showing an inverse correlation with melatonin in men (ρ = −0.52, p = 0.006), while XDO activity correlated positively with melatonin in women at 14:00 (ρ = 0.48, p = 0.01). These findings indicate sex-specific and time-dependent regulation of XOR isoforms, suggesting that redox homeostasis is modulated differently in men and women throughout the day. Understanding these dynamics may refine the interpretation of oxidative stress biomarkers and help optimize diagnostic and chronotherapeutic approaches in redox-related disorders.

Oxidative stress is characterized by an excessive concentration of reactive oxygen species (ROS) resulting from a disturbance in the balance between ROS production and their removal by antioxidant systems (SOD, CAT, GPx). Prolonged and intense oxidative stress can cause various forms of damage to cells, which markers are total antioxidant capacity (TAC), reactive oxygen species modulator (ROMO1), and malondialdehyde (MDA). It has been demonstrated that magnetic fields can positively affect human health, for example, by reducing oxidative stress. Determination of the effect of a rotating magnetic field (RMF) on the activity/concentration of selected oxidative stress markers. A group of 30 healthy volunteers (15 women and 15 men) (mean age 24.8 ± 5.1) in the study classified into the following groups: internal control group (CG);1 h 25 Hz (samples placed in the field for one hour at 25 Hz); 3 h 25 Hz (samples placed in the field for 3 h at 25 Hz), the 1 h 50 Hz group ( placed in RMF for an hour at 50 Hz), and a group of 3 h 50 Hz (samples placed in the field for 3 h at 50 Hz). Serum samples were collected in K 2 EDTA tubes.. The magnetic induction value obtained for RMF is 37.06 mT and 42.64 mT.Activity/concentration of selected oxidative stress markers was analyzed by ELISA. The influence of an RMF on the activity/concentration of SOD, MDA, TAC, and ROMO1 was demonstrated (p < 0.001; p = 0.0013; p < 0.001; p = 0.003). The RFM can reduce oxidative stress, as evidenced by higher SOD and CAT activities in the CG than in samples placed in the RFM. Prolonged exposure to the RFM at 50 Hz increased the TAC level, indicating an intensification of oxidative stress in these samples. The optimal conditions for staying in the RFM (reducing oxidative stress) are 1 h 50 Hz for SOD and MDA; 3 h 25 Hz for CAT and TAC. In the case of ROMO1, it is stated that 1 h 25 Hz are the optimal conditions for no increased production of ROS.

Platelets are the first to reach the site of tissue damage and secrete substances like platelet growth factors (GFs), which perform many different functions in the human body. Many studies suggest that GFs such as transforming GF (TGF), platelet‐derived GF (PDGF), or insulin‐like GF‐1 (IGF‐1) may be markers of survival, disease severity, and post‐coronavirus disease (COVID) complications. The study aimed to analyze the concentration of TGF‐ β , IGF‐1, and PDGF‐BB in COVID‐19 patients compared to the control group (GK). The study group consisted of 50 patients (23 men and 27 women) at the time of COVID‐19 detection, 7 days after detection, then 14 and 28 days after detecting severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection. The GK comprised 48 healthy volunteers (25 women and 23 men). IGF‐1, TGF‐ β , and PDGF‐BB concentrations in blood serum by enzyme‐linked immunosorbent assay (ELISA) methods. There was a statistically significant relationship between the concentration of IGF‐1, TGF‐ β 1, and PDGF‐BB in the study group (I–IV blood draw) and the GK ( p < 0.001). Statistical analysis showed a significant effect on the survival of COVID‐19 patients on IGF‐1 ( p = 0.013), TGF‐ β ( p = 0.013), and PGDF‐BB ( p = 0.015) levels. The analysis showed a significant effect of COVID‐19 symptom severity on IGF‐1 levels ( p = 0.018), as well as TGF‐ β ( p = 0.044) and PDGF‐BB ( p = 0.047). In the future, GF may serve as a predictor of disease severity and the development of new treatments for COVID‐19. In later studies, the focus should be on finding the relationship of COVID‐19 pathomechanism with all the parameters to understand the processes that occur in the body during SARS‐CoV‐2 virus infection.

Introduction Chronic kidney disease (CKD) leads to irreversible changes in kidney function and structure, with over 90% of patients developing arterial hypertension (HT). Renalase, dopamine, and norepinephrine are believed to influence HT development and CKD progression. Aim of the study This study aims to measure renalase, dopamine, and norepinephrine levels in CKD patients to evaluate their potential as markers for CKD progression, HT development, and cardiovascular event risk. Materials and methods The study involved 117 CKD patients divided into four groups: 32 hemodialysis patients (before and after treatment), 31 peritoneal dialysis patients, 24 kidney transplant recipients (pre- and post-transplant), and 30 conservatively treated patients (CKD stages 2–5). A control group included 31 healthy volunteers. Levels of renalase, dopamine, and norepinephrine were measured using the ELISA method. Results The study found that CKD significantly affected renalase, dopamine, and norepinephrine levels ( p  = 0.046; p  = 0.035; p  = 0.023). The lowest renalase levels were in patients with ADPKD and HT, while the highest dopamine levels were in those with CKD due to glomerulonephritis. The lowest norepinephrine levels were observed in patients with HT and diabetes. Conclusions Levels of renalase, dopamine, and norepinephrine may indicate CKD progression, cardiovascular event risk, and patient prognosis.

Platelets are actively involved in tissue injury site regeneration by producing a wide spectrum of platelet-derived growth factors such as PDGF (platelet-derived growth factor), IGF-1 (insulin-like growth factor), TGF-β1 (transforming growth factor β), FGF (fibroblast growth factor), etc. A rotating magnetic field (RMF) can regulate biological functions, including reduction or induction regarding inflammatory processes, cell differentiation, and gene expression, to determine the effect of an RMF on the regenerative potential of platelets. The study group consisted of 30 healthy female and male volunteers (n = 15), from which plasma was collected. A portion of the plasma was extracted and treated as an internal control group. Subsequent doses of plasma were exposed to RMF at different frequencies (25 and 50 Hz) for 1 and 3 h. Then, the concentrations of growth factors (IGF-1, PDGF-BB, TGF-β1, and FGF-1) were determined in the obtained material by the ELISA method. There were statistically significant differences in the PDGF-BB, TGF-β1, IGF-1, and FGF-1 concentrations between the analyzed groups. The highest concentration of PDGF-BB was observed in the samples placed in RMF for 1 h at 25 Hz. For TGF-β1, the highest concentrations were obtained in the samples exposed to RMF for 3 h at 25 Hz and 1 h at 50 Hz. The highest concentrations of IGF-1 and FGF-1 were shown in plasma placed in RMF for 3 h at 25 Hz. An RMF may increase the regenerative potential of platelets. It was noted that female platelets may respond more strongly to RMF than male platelets.