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Background Bladder cancer (BC) is the second most prevalent malignancy of the urinary system, characterized by high recurrence rates and aggressive behavior. Although treatment modalities have advanced, patient prognosis remains poor, largely due to late-stage diagnosis, postoperative recurrence, and the development of therapy resistance. Mitophagy, a selective form of autophagy responsible for degrading dysfunctional mitochondria, is a critical mechanism for maintaining cellular homeostasis. Dysregulation of mitophagy leads to the accumulation of damaged mitochondria and is implicated in the pathogenesis of numerous diseases, including cancer. Main body This review synthesizes current understanding of the molecular mechanisms by which mitophagy regulates the initiation and progression of BC. Concurrently, we critically evaluate its context-dependent functions in disease biology and therapeutic response. The role of mitophagy in BC is dual and highly context-dependent. It can function as either a tumor promoter or a tumor suppressor, with its net effect determined by multiple factors, including tumor stage, genetic background, tumor microenvironment composition, and the extent of autophagic activation. While targeting mitophagy represents a promising therapeutic strategy, its functional duality necessitates approaches that extend beyond simple inhibition or activation. Future therapeutic development must therefore focus on precise, individualized modulation tailored to specific tumor contexts. Conclusion Mitophagy plays a multidimensional and pivotal role in BC pathogenesis and treatment response. A deeper understanding of its nuanced mechanisms not only advances the fundamental knowledge of BC pathology but also unveils innovative avenues for diagnosis and targeted therapy, offering a promising strategy to overcome current clinical challenges.

Bladder cancer (BC) is a malignant tumor characterized by a high incidence of urinary system diseases. The complex pathogenesis of BC has long been a focal point in medical research. With the robust development of epigenetics, the crucial role of epigenetic modifications in the occurrence and progression of BC has been elucidated. These modifications not only affect gene expression but also impact critical biological behaviors of tumor cells, including proliferation, differentiation, apoptosis, invasion, and metastasis. Notably, DNA methylation, an important epigenetic regulatory mechanism, often manifests as global hypomethylation or hypermethylation of specific gene promoter regions in BC. Alterations in this methylation pattern can lead to increased genomic instability, which profoundly influences the expression of proto-oncogenes and tumor suppressor genes. MiRNAs, as noncoding small RNAs, participate in various biological processes of BC by regulating target genes. Consequently, this work aims to explore the interaction mechanisms between DNA methylation and miRNAs in the occurrence and development of BC. Research has demonstrated that DNA methylation not only directly influences the expression of miRNA genes but also indirectly affects the maturation and functionality of miRNAs by modulating the methylation status of miRNA promoter regions. Simultaneously, miRNAs can regulate DNA methylation levels by targeting key enzymes such as DNA methyltransferases (DNMTs), thereby establishing a complex feedback regulatory network. A deeper understanding of the crosstalk mechanisms between DNA methylation and miRNAs in BC will contribute to elucidating the complexity and dynamics of epigenetic modifications in this disease, and may provide new molecular targets and strategies for the early diagnosis, treatment, and prognostic evaluation of BC.

CircRNAs are an important class of non-coding RNAs, which are produced via back-splicing of exons and/or intron sequences of precursor mRNAs and generally cannot be translated into proteins as they do not bind to ribosomes. There is varying evidence supporting the claim that circRNAs are abnormally expressed in cancer and play a crucial role in cancer initiation and progression. Ubiquitin is a highly stable protein that can be conjugated to target proteins. The most crucial role of ubiquitination is to mediate the degradation of substrate proteins by the proteasome. An increasing amount of evidence indicates that circRNAs are involved in the precise degradation of proteins via the ubiquitin-proteasome system. This review systematically summarizes the intricate mechanisms by which circRNAs regulate target protein ubiquitination, modulate cancerous signaling pathways, and control tumorigenesis and tumor development. Although studies are continuously uncovering additional complex interactions between circRNAs and proteins, we believe that circRNAs are promising but challenging molecules that have the potential to facilitate precise cancer therapies in the future.

Chronic prostatitis is a prevalent urological condition that significantly impacts patients’ quality of life. Advances in the study of Extracellular Vesicles (EV) have revealed their close involvement in the pathogenesis of prostatitis. This paper reviews the progress in understanding the role of EV in the pathogenesis of chronic prostatitis type IIIA, particularly their involvement in inflammatory responses, cell signaling, and interactions with immune cells. Additionally, it explores the potential applications of EV as drug delivery vehicles, including the targeted delivery of anti-inflammatory agents and immunomodulators, and highlights the challenges associated with developing exosome-based therapeutic strategies. In-depth research on EV holds promise for offering new insights into the diagnosis and treatment of inflammatory diseases.

The ubiquitin (Ub) system has been demonstrated to play a crucial role in various cellular processes, including immune responses, cell development, and programmed cell death. Ubiquitination, a form of post-translational modification, occurs in eukaryotic cells and involves several key components, such as Ub-activating enzymes, Ub-binding enzymes, and Ub-protein ligases. Recently, deubiquitinating enzymes—proteases that reverse the modification of proteins by removing Ub or Ub-like molecules, or by remodeling Ub chains on target proteins—have been identified as significant regulators of ubiquitination-mediated degradation. These enzymes profoundly influence cellular pathways and numerous biological processes, including the DNA damage response and DNA repair mechanisms. Recent studies increasingly demonstrate a relationship between ubiquitination, deubiquitination, and urinary diseases. The roles of these processes in urinary diseases are complex, encompassing various aspects of signaling, protein stability, and cellular metabolism. As research advances, the specific mechanisms by which these processes influence urologic diseases will be further clarified. This review examines recent discoveries in this field, aiming to provide new strategies and targets for the diagnosis and treatment of urologic diseases.

Urologic malignancies, characterized by their high aggressiveness and metastatic potential, pose a significant public health challenge globally. Ferroptosis, a novel mode of cell death, typically arises from intracellular iron ion overload and the accumulation of lipid peroxides. This process has been shown to play a crucial regulatory role in various pathological conditions, particularly in cancer, including urologic cancers. However, the comprehensive regulatory mechanisms underlying ferroptosis remain poorly understood, which somewhat limits its broader application in cancer therapy. Non-coding RNAs (ncRNAs), which encompass microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), are non-coding transcripts that play pivotal roles in various physiological processes, such as proliferation, differentiation, apoptosis, and cell cycle regulation, by modulating the expression of target genes. The biological functions and potential regulatory mechanisms of ncRNAs in the context of cancer-related ferroptosis have been partially elucidated. Research indicates that ncRNAs can influence the progression of urologic cancers by affecting cell proliferation, migration, and drug resistance through the regulation of ferroptosis. Consequently, this review aims to clarify the functions and mechanisms of the ncRNA-ferroptosis axis in urologic cancers and to evaluate the clinical significance of ferroptosis-related ncRNAs, thereby providing new insights into cancer biology and therapeutic strategies that may ultimately benefit a diverse range of cancer patients.

Tumors of the urinary system primarily encompass prostate, bladder, and kidney cancers, which exhibit high morbidity and mortality rates worldwide and pose a particularly significant threat to men’s health. Given the associated high morbidity and mortality, early diagnosis and effective treatment are crucial. Consequently, innovative research is urgently needed to enhance the clinical care of patients with urologic cancers. Recent studies have demonstrated that microRNAs (miRNAs), as key non-coding RNA molecules that regulate gene expression, play a vital regulatory role in malignant tumor development by binding to the mRNA 3′-UTR region. Large-scale genomic analyses (e.g., TCGA Pan-Cancer Atlas) reveal that over 50% of miRNA genes reside in cancer-associated regions, regulating >60% of protein-coding genes. miR-145 exemplifies this paradigm, with its dysregulation causally linked to tumor proliferation, metastasis, and therapy resistance. Among them, miR-145, as a regulatory molecule with significant anticancer properties, presents unique expression characteristics and functional mechanisms in urological tumours. In this review, we summarize the role of miR-145 in specific urological tumors, along with its downstream target molecules and cells, which may enhance our understanding of miR-145 in these cancers. In conclusion, miR-145 is a multifaceted regulator in urological oncology that has strong potential to range from non-invasive biomarker discovery to therapeutic strategies that work synergistically with conventional treatments, ultimately advancing precision medicine in prostate, bladder, and kidney cancers.

The three most common kinds of urologic malignancies are prostate, bladder, and kidney cancer, which typically cause substantial morbidity and mortality. Early detection and effective treatment are essential due to their high fatality rates. As a result, there is an urgent need for innovative research to improve the clinical management of patients with urologic cancers. A type of small noncoding RNAs of 22 nucleotides, microRNAs (miRNAs) are well-known for their important roles in a variety of developmental processes. Among these, microRNA-21 (miR-21) stands out as a commonly studied miRNA with implications in tumorigenesis and cancer development, particularly in urological tumors. Recent research has shed light on the dysregulation of miR-21 in urological tumors, offering insights into its potential as a prognostic, diagnostic, and therapeutic tool. This review delves into the pathogenesis of miR-21 in prostate, bladder, and renal cancers, its utility as a cancer biomarker, and the therapeutic possibilities of targeting miR-21.

Urologic oncology is a significant public health concern on a global scale. Recent research indicates that long chain non-coding RNAs (lncRNAs) and autophagy play crucial roles in various cancers, including urologic malignancies. This article provides a summary of the latest research findings, suggesting that lncRNA-mediated autophagy could either suppress or promote tumors in prostate, kidney, and bladder cancers. The intricate network involving different lncRNAs, target genes, and mediated signaling pathways plays a crucial role in urological malignancies by modulating the autophagic process. Dysregulated expression of lncRNAs can disrupt autophagy, leading to tumorigenesis, progression, and enhanced resistance to therapy. Consequently, targeting particular lncRNAs that control autophagy could serve as a dependable diagnostic tool and a promising prognostic biomarker in urologic oncology, while also holding potential as an effective therapeutic approach.

Kidney stones are a globally prevalent urological disease, with calcium oxalate stones being the most common type. Their pathogenesis is complex, and postoperative recurrence rates are high. The calcium-sensing receptor (CaSR) and solute carrier family 26 member 6 (SLC26A6) play key roles in hypercalciuria and hyperoxaluria, respectively. However, the intrinsic relationship and regulatory mechanism between them in kidney stone formation remain unclear. This study aims to investigate whether CaSR regulates SLC26A6 expression through a specific signaling pathway, thereby playing a role in experimental calcium oxalate kidney stone formation in rats. , a calcium oxalate kidney stone model was established in Wistar rats by intragastric administration of 1% ethylene glycol (E.G.,) and 1% ammonium chloride. Rats were divided into six groups: blank control (NC), E.G., model (E.G.,), CaSR agonist (CaSR-a), CaSR inhibitor (CaSR-i), protein kinase A inhibitor (PKA-i), and Forkhead box protein O4 inhibitor (FOXO4-i) groups. Urinary calcium and oxalate levels were measured. Kidney crystal formation was observed via Hematoxylin and Eosin (HE) staining and Pizzolato's staining. Protein and mRNA expression of CaSR, p-protein kinase A (PKA) substrate, p-FOXO4 (Thr451), and SLC26A6 in kidney tissues were detected by Western blotting, immunohistochemistry, and Real-Time quantitative PCR (RT-qPCR). , rat renal tubular epithelial cells (NRK-52E) were intervened with calcium oxalate monohydrate (COM) crystals and treated with agonists or inhibitors of CaSR, PKA, and Forkhead box protein O4 (FOXO4). Pathway-related protein expression was detected by Western blotting. A dual-luciferase reporter gene assay was used to validate the transcriptional regulation of the SLC26A6 promoter by FOXO4. Compared to the NC group, the, E.G., group showed significantly increased urinary calcium and oxalate concentrations, increased renal crystal deposition, and upregulated expression of CaSR, p-PKA substrate, p-FOXO4, and SLC26A6. Activating CaSR (CaSR-a group) further exacerbated these phenomena, whereas inhibiting CaSR (CaSR-i group), PKA (PKA-i group), or FOXO4 (FOXO4-i group) significantly alleviated crystal formation and reduced SLC26A6 expression. Cell experiments confirmed that activating CaSR enhanced PKA and FOXO4 phosphorylation and SLC26A6 expression; activating PKA enhanced FOXO4 phosphorylation and SLC26A6 expression; activating FOXO4 upregulated SLC26A6 expression. The dual-luciferase reporter gene assay showed that FOXO4 functionally regulates SLC26A6 promoter and regulates its transcriptional activity. During the formation of experimental calcium oxalate kidney stones in rats, CaSR activation promotes PKA-mediated FOXO4 phosphorylation, leading to upregulation of SLC26A6 expression through transcriptional mechanisms. This signaling axis promotes urinary oxalate excretion and contributes to kidney stone formation. This study reveals the potential role of the novel CaSR-PKA-FOXO4-SLC26A6 signaling pathway in the pathogenesis of kidney stones.