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Diabetic nephropathy (DN) is a leading cause of end-stage renal disease, characterized by progressive kidney dysfunction. Early detection and targeted therapies remain key challenges in managing DN. This study aims to identify proteomic alterations in DN patients compared to healthy controls, focusing on proteins involved in inflammation, oxidative stress, immune response, and metabolic dysregulation. Using mass spectrometry and advanced bioinformatics, we identified significant upregulation of proteins associated with platelet activation, immune regulation, and extracellular matrix remodeling, as well as downregulation of proteins linked to lipid metabolism, immune regulation, and structural stability. These findings highlight the molecular complexity of DN and suggest that altered protein expression plays a critical role in the progression of kidney damage. The identified proteins may serve as potential biomarkers for early diagnosis and therapeutic targets for DN. Our results underline the importance of proteomic analyses in advancing the understanding of DN pathogenesis and in developing strategies for personalized treatment to improve patient outcomes. Future research should focus on further elucidating these molecular mechanisms and their implications for clinical management.

Osteoarthritis (OA) represents a degenerative joint disease which advances through cartilage breakdown, synovial inflammation, and subchondral bone transformation until it causes persistent pain and mobility loss. The scientific community lacks complete knowledge about OA disease mechanisms and post-operative healing processes despite arthroplasty surgery providing effective symptom relief. This study investigated plasma proteomic changes in OA patients before and after arthroplasty. The cohort included eight OA patients undergoing knee or hip arthroplasty and ten age-, sex-, and body mass index-matched healthy controls. Plasma proteins were analyzed using liquid chromatography–tandem mass spectrometry following enzymatic digestion and depletion of high-abundance components. The bioinformatic analysis together with quantitative methods showed that OA patients experienced changes in inflammatory pathways, extracellular matrix remodeling, immune system regulation and coagulation processes. A total of 93 proteins were differentially abundant in the pre-operative comparison. Among these, 63 proteins were consistently up-regulated and 23 were consistently down-regulated across both pre- and post-operative time points. In addition, 20 proteins exhibited post-operative-specific changes. These findings highlight both persistent disease-associated alterations and transient proteomic shifts linked to post-operative recovery. Overall, this study identifies candidate plasma proteomic signatures associated with OA and surgical intervention, providing exploratory insights into disease monitoring and potential personalized therapeutic strategies.

Decoy receptor 3 (DcR3) is a supermember of tumor necrosis receptor (TNF) factor. DcR3 acts as a binding partner in multiple apoptotic ligands that inhibit apoptosis. TNF-associated apoptosis-inducing ligand (TRAIL)-induced apoptosis has been demonstrated to be sensitized by DcR3. DcR3 has been found to be a \"pleiotropic\" soluble factor with \"decoy\" and \"non-decoy\" activities that control cell functions. The connection between Fas and FasL can be inhibited by recombinant DcR3 coupled with an IgG1 Fc domain. TNF superfamily FasL can inhibit apoptosis and increase angiogenesis through neutralizing members of LIGHT and TL1A. DcR3 serum level is almost undetectable in most normal individuals without inflammatory diseases and cancer. According to several research, the level of DcR3 in the blood is linked to cancer stage in cancer patients. High DcR3 levels in serum or tissues have been found to be associated with poor prognosis and/or resistance to therapy in some cancer patients. As a result, identifying the cut-off value of the DcR3 serum level will provide to able to forecast the severity of disease in the future. While inhibiting DcR3 expression may slow tumor growth, improving DcR3-mediated effector functions could be a viable strategy for reducing autoimmunity and promoting tissue healing. Thus, recombinant DcR3 is a promising immunotherapeutic agent; yet, in the malignant environment, turning off DcR3 expression may improve cancer therapy success. The purpose of this review is to provide clinical convenience by collecting the findings of studies on DcR3 so far. These discoveries could help with cancer diagnosis, differentiation, metastasis, and stage detection. Furthermore, these may provide new therapeutic approaches to target carcinomas in the future.

This study aimed to evaluate the inhibitory potential of phenolic-rich extracts from selected medicinal plants belonging to the Lamiaceae and Asteraceae families against the furin protease enzyme, a key target in viral and oncogenic pathways. Extracts of Origanum vulgare, Thymus vulgaris, Mentha piperita, Mentha spicata, Salvia officinalis, and Silybum marianum were prepared using hexane, chloroform, and ethyl acetate. Phenolic compounds were quantified using High-Performance Liquid Chromatography (HPLC). Furin inhibition was assessed spectrophotometrically and analyzed statistically with multivariate approaches. The chloroform extract of Origanum vulgare exhibited 97.44 ± 0.12% inhibition, while the ethyl acetate extract of Mentha spicata showed 97.44 ± 0.08% inhibition. Epicatechin and rutin displayed significant synergistic effects, while naringenin negatively affected inhibition (p < 0.05). Solvent polarity significantly influenced phenolic diversity and biological activity, with ternary combinations showing 33% higher inhibition than single compounds. These findings highlight phenolic blends as promising natural furin inhibitors, with chloroform being optimal for broad-spectrum extraction.

Degenerative joint disease is a condition that affects joints and is commonly referred to as osteoarthritis (OA). This form of arthritis is most prevalent among women and tends to become more frequent as people age. The pathogenesis of OA involves an imbalance of cytokines in favor of pro-inflammatory cytokines. However, the steroid hormone dehydroepiandrosterone (DHEA) exerts chondroprotective effects and regulates the balance of catabolic factors such as thrombospondin motif disintegrin and metalloproteinase (ADAMTS), thereby playing a role against OA. Pro-inflammatory cytokines induce aggrecanases, such as ADAMTS5, which degrade the extracellular matrix and contribute to OA. The molecule nerve growth factor (NGF), associated with pain in OA, is important for cartilage homeostasis, and DHEA can modulate pain by interfering with NGF receptors. This review covers the roles of DHEA, ADAMTS5, and NGF in the pathogenesis of OA, their relationship with pain pathways, and their use in current treatments. We also anticipate that these pathways will be crucial in developing new strategies to prevent and treat OA, and understanding their interactions may make it possible to enhanced the quality of life of patients with OA.

Background The incidence of non-alcoholic fatty liver disease (NAFLD) is increasing with obesity, and it is believed that the ongoing low-grade inflammation in obesity and alterations in the enterohepatic axis contributing this process. This study aimed to determine the role of fecal calprotectin (FC) as inflammatory biomarker in obesity and NAFLD. Methods Between November 2022-August 2023, 31 obese and 10 healthy adolescents aged between 10 and 18 years enrolled in this prospective controlled study. Body mass index higher than 2 standard deviation is considered as obesity. Obese adolescents were divided into two subgroups: obese adolescents ( n  = 11) and Obese + NAFLD group ( n  = 20). NAFLD diagnosis was made with biochemical analysis or ultrasonography. FC levels and laboratory parameters analyzed in study group, while only FC samples taken from control group. Anthropometric and laboratory parameters were compared between groups. This study was registered in ClinicalTrials.gov (NCT06229184). Results The median (IQR P25-75) FC levels in the obese + NAFLD, obese and the healthy controls were 136.23 (43.36-332.04), 61.77 (29.70-285.92) and 38.95 (27.59–50.52) µg/g feces, respectively ( p  = 0.018). Subgroup analyses revealed that the significant difference was between the obese + NAFLD group and the control group ( p  = 0.02), while no significant differences were observed between the control and obese groups, or between the obese and obese + NAFLD groups. FC positivity rates were 20% ( n  = 2) in the control group, 54.5% ( n  = 6) in the obese group, and 75% ( n  = 15) in the Obese + NAFLD group ( p  = 0.018). Conclusions FC is significantly higher in obese adolescents compared to healthy peers, but no significant difference was observed between obese and obese + NAFLD groups. Further studies needed on this subject. Trial registration This trial is registered in ClinicalTrials.gov (Trial registration number [ClinicalTrials.gov ID] NCT06229184).

Decoy receptor 3 (DcR3) is a supermember of tumor necrosis receptor (TNF) factor. DcR3 acts as a binding partner in multiple apoptotic ligands that inhibit apoptosis. TNF-associated apoptosis-inducing ligand (TRAIL)-induced apoptosis has been demonstrated to be sensitized by DcR3. DcR3 has been found to be a ‘‘pleiotropic’’ soluble factor with ‘‘decoy’’ and ‘‘non-decoy’’ activities that control cell functions. The connection between Fas and FasL can be inhibited by recombinant DcR3 coupled with an IgG1 Fc domain. TNF superfamily FasL can inhibit apoptosis and increase angiogenesis through neutralizing members of LIGHT and TL1A. DcR3 serum level is almost undetectable in most normal individuals without inflammatory diseases and cancer. According to several research, the level of DcR3 in the blood is linked to cancer stage in cancer patients. High DcR3 levels in serum or tissues have been found to be associated with poor prognosis and/or resistance to therapy in some cancer patients. As a result, identifying the cut-off value of the DcR3 serum level will provide to able to forecast the severity of disease in the future. While inhibiting DcR3 expression may slow tumor growth, improving DcR3-mediated effector functions could be a viable strategy for reducing autoimmunity and promoting tissue healing. Thus, recombinant DcR3 is a promising immunotherapeutic agent; yet, in the malignant environment, turning off DcR3 expression may improve cancer therapy success. The purpose of this review is to provide clinical convenience by collecting the findings of studies on DcR3 so far. These discoveries could help with cancer diagnosis, differentiation, metastasis, and stage detection. Furthermore, these may provide new therapeutic approaches to target carcinomas in the future.

Degenerative joint disease is a condition that affects joints and is commonly referred to as osteoarthritis (OA). This form of arthritis is most prevalent among women and tends to become more frequent as people age. The pathogenesis of OA involves an imbalance of cytokines in favor of pro-inflammatory cytokines. However, the steroid hormone dehydroepiandrosterone (DHEA) exerts chondroprotective effects and regulates the balance of catabolic factors such as thrombospondin motif disintegrin and metalloproteinase (ADAMTS), thereby playing a role against OA. Pro-inflammatory cytokines induce aggrecanases, such as ADAMTS5, which degrade the extracellular matrix and contribute to OA. The molecule nerve growth factor (NGF), associated with pain in OA, is important for cartilage homeostasis, and DHEA can modulate pain by interfering with NGF receptors. This review covers the roles of DHEA, ADAMTS5, and NGF in the pathogenesis of OA, their relationship with pain pathways, and their use in current treatments. We also anticipate that these pathways will be crucial in developing new strategies to prevent and treat OA, and understanding their interactions may make it possible to enhanced the quality of life of patients with OA.

Heart failure (HF) has a high prevalence and mortality rate in elderly patients; however, there are few studies that have focused on patients older than 80 years. The aim of this study is to describe and compare the age-specific demographics and clinical features of Turkish elderly patients with HF who were admitted to cardiology clinics. The Epidemiology of Cardiovascular Disease in Elderly Turkish population (ELDER-TURK) study was conducted in 73 centers in Turkey, and it recruited a total of 5694 patients aged 65 years or older. In this study, the clinical profile of the patients who were aged 80 years or older and those between 65 and 79 years with HF were described and compared based on the ejection fraction (EF)-related classification: HFrEF and HFpEF (is considered as EF: ≥50%). A total of 1098 patients (male, 47.5%; mean age, 83.5+-3.1 years) aged ≥80 years and 4596 patients (male, 50.2 %; mean age, 71.1+-4.31 years) aged 65-79 years were enrolled in this study. The prevalence of HF was 39.8% for patients who were ≥80 years and 27.1% for patients 65-79 years old. For patients aged ≥80 years with HF, the prevalence rate was 67% for hypertension (HT), 25.6% for diabetes mellitus (DM), 54.3% for coronary artery disease (CAD), and 42.3% for atrial fibrilation. Female proportion was lower in the HFrEF group (p=0.019). The prevalence of HT and DM was higher in the HFpEF group (p<0.01), whereas CAD had a higher prevalence in the HFrEF group (p=0.02). Among patients aged 65-79 years, 43.9% (548) had HFpEF, and 56.1% (700) had HFrEF. In this group of patients aged 65-79 years with HFrEF, the prevalence of DM was significantly higher than in patients aged ≥80 years with HFrEF (p<0.01). HF is common in elderly Turkish population, and its frequency increases significantly with age. Females, diabetics, and hypertensives are more likely to have HFpEF, whereas CAD patients are more likely to have HFrEF.