Organ fibrosis is a progressive and often irreversible pathological process characterized by excessive deposition of extracellular matrix, leading to tissue dysfunction and failure. Despite its significant impact on various organ systems, available antifibrotic therapies remain limited. This review focuses on novel therapeutic approaches to inhibit fibrosis and improve clinical outcomes. Current strategies include small molecule inhibitors, monoclonal antibodies targeting fibrosis mediators, gene therapies, and cell-based approaches, including mesenchymal stem cells and induced pluripotent stem cells. In addition, the development of innovative drug delivery systems and combination therapies involving pulsed magnetic fields (PMFs) opens new possibilities for increasing the precision and efficacy of treatment. In recent years, multiomic approaches have enabled a better understanding of fibrosis mechanisms, facilitating the personalization of therapy. The role of artificial intelligence in drug discovery has also increased, as exemplified by models that support the design of small-molecule inhibitors currently undergoing clinical evaluation. This review discusses key signaling pathways involved in fibrosis progression, such as TGF-β, p38 MAPK, and fibroblast activation, as well as novel therapeutic targets. Although clinical trial results indicate promising potential for new therapies, challenges remain in optimizing drug delivery, considering patient heterogeneity, and ensuring long-term safety. The future of fibrosis therapy relies on integrating precision medicine, combination therapies, and molecularly targeted strategies to inhibit or even reverse the fibrosis process. Further intensive interdisciplinary collaboration is required to successfully implement these innovative solutions in clinical practice.

Background: Upper tract urothelial carcinoma (UTUC) is a rare malignancy representing approximately 5–10% of all urothelial cancers. Key risk factors include smoking, chemical exposures, selected metabolic conditions, and hereditary cancer syndromes. This narrative review summarises current knowledge on UTUC molecular pathogenesis, major risk determinants, and contemporary therapeutic strategies. Methods: This study was conducted as a narrative review with a structured literature search. PubMed, Web of Science, Embase, and Scopus were searched using predefined combinations of UTUC-related terms covering molecular pathogenesis, carcinogenic risk factors, and treatment strategies. The review was prepared according to SANRA principles to improve transparency and consistency; however, no formal systematic review methodology or meta-analysis was performed. Results: Available genomic studies indicate that UTUC has a molecular profile distinct from urothelial bladder carcinoma (UBC), with recurrent alterations involving FGFR3, HRAS, KMT2D, CDKN2A, KRAS, MYC, and BRIP1. Smoking, aristolochic acid exposure, Lynch syndrome, and possibly early-onset urolithiasis contribute to carcinogenesis through distinct but incompletely understood mechanisms. Surgical treatment remains the standard of care for high-risk localised disease, whereas perioperative chemotherapy, immunotherapy, and targeted agents are expanding treatment options, particularly in advanced disease. A substantial proportion of the therapeutic evidence, however, is derived from broader urothelial carcinoma populations rather than UTUC-specific studies. Conclusions: UTUC is biologically heterogeneous and shaped by both molecular alterations and environmental exposures. Although substantial progress has been made, important gaps remain in understanding UTUC-specific carcinogenic mechanisms and in defining evidence-based personalised treatment strategies. Better integration of molecular, environmental, and clinical data is needed to improve risk stratification and treatment selection.

Background: It is estimated that approximately 20–30% of women suffer from recurrent urinary tract infections (rUTIs). The disease is primarily bacterial, especially Escherichia coli, making antibiotics the standard treatment. Increasing antibiotic resistance of uropathogens reduces treatment effectiveness. Therefore, non-antibiotic approaches are increasingly being investigated for the management of rUTIs. This narrative review provides a comprehensive overview of currently available and emerging methods of treatment and prevention of rUTIs in women. Methods: This paper employs a narrative review with a structured literature search and synthesizes data from three major databases, including PubMed, Web of Science, and Scopus. The review was conducted in accordance with the Scale for the Assessment of Narrative Review Articles (SANRA) checklist. Scientific articles were searched using the following keywords: ‘recurrent urinary tract infections in women’, ‘antibiotic prophylaxis’, ‘immunoprophylaxis’, ‘urinary microbiome’. Results: Observational evidence has reported an association between continuous antibiotic prophylaxis and severe outcomes, including pyelonephritis and septicemia; however, these findings are susceptible to confounding by indication and should not be interpreted as evidence of a causal relationship. Clinical studies suggest that immunomodulatory approaches, such as OM-89 bacterial lysate, next-generation polybacterial mucosal vaccines (e.g., MV140), and oral immunostimulants, have potential to reduce the frequency of rUTI recurrences in women, although the strength and certainty of evidence vary between interventions. Bacteriophage therapy is an emerging and exploratory targeted approach supported by early clinical and experimental evidence, but its efficacy for preventing recurrent uncomplicated UTIs remains uncertain, though rapid development of phage resistance remains a potential limitation. Prophylactic strategies, including Lactobacillus-based probiotics, low-dose estriol, and microbiota transplantation, have shown preliminary or variable results, with limited evidence for rUTI prevention. In particular, findings on vaginal dysbiosis and microbiota modulation should not be interpreted as a direct evidence of rUTI prevention. Conclusions: While antibiotic therapy remains essential, continuous prophylaxis may contribute to antimicrobial resistance and disrupt microbial balance. Therefore, novel therapeutic strategies are still being studied. Several non-antibiotic strategies, including immunoprophylaxis and microbiome modulation, represent potential preventive approaches, whereas bacteriophage therapy and vaginal microbiota transplantation remain exploratory and require further clinical validation. Their preventive efficacy against rUTIs remains unestablished. Moreover, antimicrobial peptides (AMPs), nanotechnology, molecularly targeted therapies, and precision medicine strategies are being investigated. Plant-based therapies may provide benefit, but their clinical efficacy remains to be established. Overall, further clinical studies are needed to confirm the preventive efficacy of these emerging approaches.