Background: The role of glycolysis in tumorigenesis has received increasing attention and multiple glycolysis-related genes (GRGs) have been proven to be associated with tumor metastasis. Hence, we aimed to construct a prognostic signature based on GRGs for clear cell renal cell carcinoma (ccRCC) and to explore its relationships with immune infiltration. Methods: Clinical information and RNA-sequencing data of ccRCC were obtained from The Cancer Genome Atlas (TCGA) and ArrayExpress datasets. Key GRGs were finally selected through univariate COX, LASSO and multivariate COX regression analyses. External and internal verifications were further carried out to verify our established signature. Results: Finally, 10 GRGs including ANKZF1, CD44, CHST6, HS6ST2, IDUA, KIF20A, NDST3, PLOD2, VCAN, FBP1 were selected out and utilized to establish a novel signature. Compared with the low-risk group, ccRCC patients in high-risk groups showed a lower overall survival (OS) rate (P = 5.548Ee-13) and its AUCs based on our established signature were all above 0.70. Univariate/multivariate Cox regression analyses further proved that this signature could serve as an independent prognostic factor (all P < 0.05). Moreover, prognostic nomograms were also created to find out the associations between the established signature, clinical factors and OS for ccRCC in both the TCGA and ArrayExpress cohorts. All results remained consistent after external and internal verification. Besides, nine out of 21 tumor-infiltrating immune cells (TIICs) were highly related to high- and low- risk ccRCC patients stratified by our established signature. Conclusions: A novel signature based on 10 prognostic GRGs was successfully established and verified externally and internally for predicting OS of ccRCC, helping clinicians better and more intuitively predict patients’ survival.

Introduction: Ureteral stricture caused by iatrogenic ureteral injury induced ureteral injury is more common and challenging to recover quickly. The effective prevention of ureteral stricture due to iatrogenic ureteral injury-induced ureteral damage is a current challenge for urologists. The purpose of this study was to evaluate the effectiveness of nanoparticle/pirfenidone complex-coated ureteral stents with slow-release pirfenidone for the prevention of ureteral stricture in rabbits. In this study, we developed a nanoparticle/pirfenidone complex-coated ureteral stent to deliver pirfenidone into the injured ureter to inhibit ureteral stricture. Methods: Twelve New Zealand rabbits were divided into four groups: Sham, US, US+ Unmodified ureteral stent, and US+NP/PFD ureteral stent; we constructed an irreversible electroporation model of ureteral injury in rabbits and placed unmodified ureteral stents and nanoparticle/pirfenidone complex-coated ureteral stents into the ureter. Two weeks later, we euthanized the rabbits and removed their bilateral kidneys and ureters. We evaluated the effect of ureteral stent prophylaxis by gross specimen observation, section staining, and Western Blot. Results: We found that the nanoparticle/pirfenidone complexes could adhere uniformly to the surface of the ureteral stent. After placement into the ureter, the nanoparticle/pirfenidone complexes were able to remain on the surface of the ureteral stent. We found nanoparticle/pirfenidone complexes could diffuse in the ureteral epithelial tissue two weeks after the order. The study showed that nanoparticle/pirfenidone complex-coated ureteral stents placed into the ureter showed significantly less stenosis due to fibrosis than in US control rabbits and rabbits treated with unmodified ureteral stents. Conclusion: We used a novel platform based on nanoparticle/pirfenidone complex-coated ureteral stents for local and sustained delivery of pirfenidone, which can effectively deliver pirfenidone to the tissue and can slowly control the release of pirfenidone. Therefore, combining ureteral stents with nanoparticle/pirfenidone complexes was an effective measure to prevent ureteral stricture.

Background: This study was designed to establish a sensitive prognostic model based on apoptosis-related genes to predict overall survival (OS) in patients with clear cell renal cell carcinoma (ccRCC).Methods: Obtaining the expression of apoptosis-related genes and associated clinical parameters from online datasets (The Cancer Genome Atlas, TCGA), their biological function analyses were performed through differently expressed genes. By means of LASSO, unadjusted and adjusted Cox regression analyses, this predictive signature was constructed and validated by internal and external databases (both TCGA and ArrayExpress).Results: A total of nine apoptosis-related genes (SLC27A2, TNFAIP2, IFI44, CSF2, IL4, MDK, DOCK8, WNT5A, APP) were ultimately screened as associated hub genes and utilized to construct a prognosis model. Then our constructed riskScore model significantly passed the validation in both the internal and external datasets of OS (all p < 0.05) and verified their expressions by qRT-PCR. Moreover, we conducted the Receiver Operating Characteristic (ROC), finding the area under the ROC curves (AUCs) were all above 0.70 which indicated that riskScore was a stable independent prognostic factor (p < 0.05). Furthermore, prognostic nomograms were established to figure out the relationship between 1-, 3- and 5-year OS and individual parameters for ccRCC patients. Additionally, survival analyses indicated that our riskScore worked well in predicting OS in subgroups of age, gender, grade, stage, T, M, N0, White (all p < 0.05), except for African, Asian and N1 (p > 0.05). We also explored its association with immune infiltration and applied cMap database to seek out highly correlated small molecule drugs.Conclusion: Our study successfully constructed a prognostic model containing nine hub apoptosis-related genes for ccRCC, helping clinicians predict patients’ OS and making the prognostic assessment more standardized. Future prospective studies are required to validate our findings.

The aim of this article was to construct an accurate prognostic model by using RNA-binding proteins (RBPs) to predict overall survival (OS) for patients with clear cell renal cell carcinoma (ccRCC) as well as to reveal its associations with immune infiltration. Expression profiles based on RNA-binding proteins (RBPs) and clinical follow-up parameters were obtained from the Cancer Genome Atlas (TCGA) and the ArrayExpress databases. Through univariate COX and LASSO regression analyses, the RBPs based signature was developed. A total of six RBPs (CLK2, IGF2BP2, RNASE2, EZH2, PABPC1L, RPL22L1) were eventually used to establish a prognostic signature. Based on this signature, ccRCC patients were classified into high-risk and low-risk subgroups and significant OS was obtained in both the internal and external datasets (p<0.05). AUCs of its ROC curve were all above 0.70 and this signature was an independent prognostic factor of OS for ccRCC (p<0.05). Nomograms were also constructed to visualize the relationships among individual predictors and 1-, 3- and 5-year OS for ccRCC. Furthermore, the established RBPs based signature was strongly related to critical clinicopathologic characteristics such as grade (p=8.921e−12), stage (p=1.421e−11), M (p=1.662e−05), and T stage (p=7.907e−10). Moreover, 12 kinds of tumor-infiltrating immune cells were significantly linked to high-risk and low-risk groups classified by our constructed model (all p<0.05). Our study successfully identified six RBPs as a robust prognostic signature in ccRCC by both external and internal verification. Besides, our established model displayed significant associations with immune infiltration. In addition to original clinical parameters, our findings may further help clinicians in predicting patients’ survival status and creating individualized treatment plans.

Atherosclerosis-induced erectile dysfunction (AED) is a common and clinically significant vascular disorder that affects men’s quality of life and serves as a potential early indicator of systemic cardiovascular disease (CVD). Atherosclerosis (AS), characterized by arterial wall inflammation, lipid accumulation, and endothelial damage, shares critical risk factors with AED, including hypertension, diabetes, hyperlipidemia, and smoking. These shared pathogenic drivers contribute to a bidirectional relationship: AS accelerates erectile dysfunction (ED) through vascular impairment, while ED often precedes overt cardiovascular events, highlighting its role as a “window” into systemic vascular health. Despite the widespread use of phosphodiesterase 5 (PDE5) inhibitors as first-line therapy, their efficacy is limited in severe cases due to persistent endothelial dysfunction, underscoring the need to clarify the vascular endothelial mechanisms underlying AED for optimized therapeutic strategies. This review systematically analyzes the role of vascular endothelial mechanisms in AED progression through a comprehensive literature synthesis. Key focuses include pathophysiological interactions between endothelial dysfunction and cavernosal hypoxia, molecular biomarkers linking AS to erectile impairment, and clinical evidence from trials evaluating endothelial-targeted therapies. Mechanistically, the decreased activity of endothelial nitric oxide synthase (eNOS)—a critical enzyme in nitric oxide (NO) production—is strongly associated with increased AED severity. Reduced NO bioavailability impairs cavernosal smooth muscle relaxation, while endothelial damage triggers inflammatory cascades, oxidative stress, and transforming growth factor-β (TGF-β)-mediated fibrosis, further exacerbating ED. Clinically, this review highlights that combining PDE5 inhibitors with endothelial repair agents (e.g., statins or anti-inflammatory therapies) enhances therapeutic effects by restoring NO signaling and mitigating vascular damage. Additionally, emerging strategies such as nanomedicine-targeted drug delivery and gene therapy show promise in protecting endothelial integrity. Collectively, these findings confirm that vascular endothelial dysfunction serves as both a key biomarker and actionable therapeutic target in AED management. Multimodal therapies addressing endothelial health not only improve erectile function but also hold potential for reducing systemic atherosclerotic risk, emphasizing a holistic approach to AED care.