Endothelial progenitor cells (EPCs), which are a type of stem cell, have been found to have strong angiogenic and tissue repair capabilities. Extracellular vesicles (EVs) contain many effective components, such as cellular proteins, microRNAs, messenger RNAs, and long noncoding RNAs, and can be secreted by different cell types. The functions of EVs depend mainly on their parent cells. Many researchers have conducted functional studies of EPC-derived EVs (EPC-EVs) and showed that they exhibit therapeutic effects on many diseases, such as cardiovascular disease, acute kidney injury, acute lung injury, and sepsis. In this review article, we comprehensively summarized the biogenesis and functions of EPCs and EVs and the potent role of EPC-EVs in the treatment of various diseases. Furthermore, the current problems and future prospects have been discussed, and further studies are needed to compare the therapeutic effects of EVs derived from various stem cells, which will contribute to the accelerated translation of these applications in a clinical setting.

Circular RNAs (circRNAs) are a novel group of endogenous RNAs with a circular structure. Growing evidence indicates that circRNAs are involved in a variety of human diseases including malignancies. CircRNA ZNF609 (circ‐ZNF609), derived from the ZNF609 gene sequence, has been demonstrated to be involved in the development and progression of many diseases. circ‐ZNF609 is thought to be a viable diagnostic and prognostic biomarker for several diseases and might be a new therapeutic target, but further research is needed to accelerate clinical application. Here, we review the biogenesis and function of circRNAs and the functional roles and molecular mechanism related to circ‐ZNF609 in neoplasms and other diseases.

Objective: We conducted this meta-analysis to examine the effect of remote ischemic conditioning (RIC) on contrast-induced acute kidney injury (CI-AKI) in patients undergoing intravascular contrast administrationon.

Renal cell carcinoma (RCC) originates from the epithelial cells of the renal tubules and has a high degree of malignancy and heterogeneity. Recent studies have found that exosomes regulate intercellular communication via transferring various bioactive molecules, such as circular RNAs (circRNAs), which are critical for cancer progression. However, the role of tumor cell-derived exosomal circRNAs in RCC remains unclear. In this study, we reported the high expression of circ-PRKCI in RCC tissues and serum exosomes. We also found that circ-PRKCI could be transferred exosomally from highly malignant RCC cells to relatively less malignant RCC cells. Tumor cell-derived exosomal circ-PRKCI promoted the proliferation, migration, and invasion of RCC cells, while inhibiting their apoptosis. Mechanistically, we found that circ-PRKCI promoted the proliferation of RCC via the miR-545-3p/CCND1 signaling pathway. Our study is the first to report the potential mechanisms of tumor cell-derived exosomal circ-PRKCI in RCC. In conclusion, this study will provide a new understanding about the molecular mechanisms of RCC progression.

Background: Polo-like kinase 1 (PLK1) belongs to polo-like kinases family and affects cell cycles. However, the role of PLK1 in some malignant tumors remains unclear. Methods: To obtain a comprehensive view of PLK1 expression patterns, public databases including The Cancer Genome Atlas, Cancer Cell Line Encyclopedia, the Genotype-Tissue Expression, and human cell landscape databases were employed. The correlation of PLK1 expression with prognosis, immune infiltrations, immune checkpoint genes, tumor mutational burden (TMB), microsatellite instability (MSI), mismatch repair (MMR), and DNA methylation was examined. Besides, we validated the results of clear cell renal cell carcinoma (ccRCC) in two cohorts, with quantitative real-time PCR, Western blot, and loss-of-function experiments. Results: By mining public datasets, we discovered that PLK1 expression in tumor tissues and cancer cell lines displayed heterogeneity compared to normal controls across different cancers. Besides, high expression of PLK1 results in shorter survival time in 15 cancer types, especially in ccRCC. PLK1 expression showed strong association with immune cell infiltration and immune checkpoint genes across cancer types. Moreover, we identified a strong association between PLK1 expression and TMB, MSI MMR, and DNA methylation. PLK1 was validated to be highly expressed in ccRCC tissues and promote ccRCC cell proliferation, migration, invasion, and cell cycle. Mechanistically, PLK1 could regulate forkhead box protein M1 and target cell cycle-associated genes to participate in cell cycle control. Conclusion: PLK1 has important prognostic value and is associated with tumor immunity across cancer types including ccRCC.

Human endogenous retroviruses (HERVs), constituting approximately 8% of the human genome, represent genomic remnants of ancestral retroviral infections that colonized the germline through evolutionary processes. While most HERVs remain epigenetically silenced, their reactivation through environmental stimuli or epigenetic dysregulation enables participation in oncogenesis via viral mimicry, immunomodulation, and insertional mutagenesis. Substantial evidence now implicates aberrant HERVs activity across urologic malignancies—including prostate cancer, renal cell carcinoma (RCC), bladder cancer, and testicular germ cell tumors—where cancer-type-specific mechanisms drive tumor development and progression. These encompass androgen-responsive HERV-K activation in prostate malignancies, hypoxia-inducible factor-mediated ERV immunogenicity in RCC, HERV-derived microRNA silencing of tumor suppressors in bladder cancer, and DNA hypomethylation-associated HERV expression in testicular germ cell tumors. This review synthesizes fundamental HERV biology with recent advances in their diagnostic and therapeutic applications for urologic neoplasms. Key clinical translations include ERV-based stratification models predicting immune checkpoint inhibitor response in metastatic RCC, HERV-E-targeted adoptive T cell therapies, and noncoding RNA biomarkers for early bladder cancer detection. We further discuss unresolved mechanistic paradoxes such as contradictory prognostic associations between HERV superfamily expression and PBRM1 inactivation in RCC, concluding with priorities for future research: validating HERV-derived neoantigens in immunotherapy platforms, optimizing epigenetic priming strategies to enhance viral mimicry effects, and establishing standardized HERV signatures as clinical biomarkers through multi-institutional cohorts.