Zinc deficiency is common in patients with liver cirrhosis, and the effects of zinc supplementation on cirrhosis remain controversial. This study aims to explore the effectiveness of zinc supplementation in the clinical treatment of cirrhosis and hepatic encephalopathy. MEDLINE, Embase, Cochrane Library, Scopus, Ovid, and Web of Science databases were searched with a cutoff date of March 2025. A meta-analysis of randomized controlled trials on the efficacy of zinc supplementation in the treatment of liver cirrhosis and hepatic encephalopathy was performed using RevMan5.4 and StataMP17 software. Seven studies comprising 338 patients with cirrhosis (172 patients in the treatment group and 166 patients in the control group) were included. Results indicated that zinc supplementation slightly increased serum albumin levels compared with those of the control group (WMD=0.07, 95
NSUN5 is a pivotal RNA 5-methylcytosine (m5C) methyltransferase that predominantly catalyzes site-specific m5C modifications in ribosomal RNA (rRNA), thereby regulating ribosome assembly, selective translation, and cellular stress adaptation. Recent studies have demonstrated that NSUN5 is aberrantly expressed in multiple cancer types, and its upregulation is often associated with advanced tumor stage, poor prognosis, and immune evasion. Mechanistically, NSUN5 modulates the m5C modification of rRNA or specific mRNAs, reshaping the cellular proteome and influencing tumor cell proliferation, migration, invasion, and stemness maintenance. Moreover, NSUN5 participates in tumor metabolic reprogramming, including glycolysis and lipid biosynthesis, as well as in cellular stress responses and resistance to chemotherapy and radiotherapy. NSUN5 can also mediate tumor microenvironmental regulation through RNA modifications, such as modulating macrophage polarization, enhancing antioxidative capacity, and facilitating immune escape. Functional crosstalk exists between NSUN5 and other RNA epigenetic regulators, forming a complex regulatory network. Given its central role and structural features, NSUN5 represents a potential therapeutic target and biomarker. Direct strategies include small-molecule inhibitors that block its methyltransferase activity, whereas indirect approaches focus on interfering with downstream signaling pathways or synergizing with other RNA modifications to inhibit tumor progression. Additionally, NSUN5 expression may serve as a stratification marker for patient classification and treatment response prediction, supporting precision oncology. Future research should focus on genome-wide target identification, integration of single-cell and spatial transcriptomics, and mechanism-driven drug development to advance the clinical translation of NSUN5-targeted interventions.
BACKGROUND:Acute myocardial infarction (AMI) is a leading global cause of death, with extracellular vesicles (EVs) emerging as potential therapeutic mediators. However, the mechanisms by which circulating EVs from different sources influence myocardial injury remain unclear. METHOD:Circulating EVs from AMI patients (AMI-EVs) and healthy controls (N-EVs) were isolated. In vitro assays (CCK8, EdU, flow cytometry, wound healing, angiogenesis) evaluated their effects on cardiomyocyte/endothelial cell proliferation, apoptosis, migration, and tube formation. Immune cell infiltration and immunoglobulin levels in myocardial injury patients were analyzed. Microarray and qPCR identified differentially expressed miRNAs in EVs. CYP1B1, predicted as a target of miR-16-5p via bioinformatics, was validated using dual-luciferase reporter and RNA co-immunoprecipitation. An ischemia-reperfusion (I/R) mouse model assessed EV effects on myocardial injury and PANoptosis. RESULT:N-EVs alleviated I/R-induced myocardial injury in vivo and protected cardiomyocytes/endothelial cells from H2O2-induced damage in vitro. Patients with myocardial injury exhibited IgG deposits, immune cell infiltration, and elevated IgG1/IgG3 levels. N-EVs promoted angiogenesis and cardiomyocyte proliferation while suppressing PANoptosis (combined apoptosis, necroptosis, pyroptosis). Mechanistically, miR-16-5p was enriched in N-EVs and directly targeted CYP1B1, inhibiting its expression and downstream PANoptosis pathways. CONCLUSION:N-EVs mitigate myocardial injury by delivering miR-16-5p to suppress CYP1B1-mediated PANoptosis, highlighting their role in intercellular communication and therapeutic potential for AMI. This study provides insights into EV-based strategies for cardiac repair and fibrosis prevention.
Neurosyphilis is a heterogeneous manifestation of Treponema pallidum infection with diverse clinical and radiological presentations. Concurrent involvement of the brain and spinal cord is rare and may mimic intracranial neoplasms, leading to diagnostic uncertainty. A 48-year-old woman presented with acute-onset limb numbness and diplopia. Brain and cervical spine magnetic resonance imaging (MRI) revealed multiple nodular and ring-enhancing lesions involving the brain parenchyma and cervical spinal cord, initially raising suspicion of lymphoma or metastatic tumors. Diffusion-weighted imaging (DWI) showed atypical hypointensity without diffusion restriction. Histopathological examination demonstrated perivascular inflammatory infiltration without evidence of malignancy. Serological testing confirmed a reactive serum rapid plasma reagin (RPR) titer with treponemal confirmation, and metagenomic next-generation sequencing (mNGS) of cerebrospinal fluid (CSF) detected Treponema pallidum deoxyribonucleic acid (DNA), supporting the diagnosis of neurosyphilis. HIV serology was negative. Due to a documented penicillin allergy (positive penicillin skin test), the patient received alternative antimicrobial therapy with fosfomycin (8 g/day intravenously) and minocycline (100 mg orally twice daily), resulting in marked clinical improvement and regression of lesions on follow-up imaging. This report describes a patient in whom neurosyphilis presented with concurrent brain and spinal cord lesions that radiologically resembled malignant central nervous system (CNS) tumors. Multifocal nodular and ring-enhancing lesions without diffusion restriction, combined with clinical improvement following antimicrobial therapy, were features observed in this case that contributed to the diagnostic re-evaluation. This case highlights the importance of including neurosyphilis in the differential diagnosis of tumor-like CNS lesions when imaging findings are atypical, while acknowledging that definitive diagnostic conclusions are limited by the single-case nature of this report.
N-acetyltransferase 10 (NAT10), the primary writer of N4-acetylcytidine (ac4C) on RNA, is broadly upregulated across multiple cancer types and correlates with tumor proliferation, invasion, therapeutic resistance, and poor prognosis, indicating its significant clinical relevance. In this mini review, we systematically summarize the functional roles and mechanisms of NAT10-mediated ac4C modification in both normal development and cancer. Specifically, we cover recent advances in the regulation of mRNA stability and translation, as well as modifications of tRNA, long non-coding RNA (lncRNA), microRNA (miRNA), and circular RNA (circRNA). Moreover, we integrate evidence supporting the essential roles of NAT10 in embryonic development, gametogenesis, stem cell self-renewal and differentiation, cellular architecture and cell cycle control, and immune cell expansion, while outlining its oncogenic contributions to tumor growth, metastasis, metabolic reprogramming, drug resistance, and immune evasion. Based on clinical findings, we discuss the potential of NAT10 as a diagnostic and prognostic biomarker and its application in liquid biopsy, and we evaluate the therapeutic potential and limitations of targeting NAT10, including toxicity, specificity, and resistance. Finally, we propose future research directions, including the tumor-specific mechanisms driving NAT10 upregulation, strategies for selectively targeting cancer versus normal physiology, identification of ac4C readers and erasers, and potential crosstalk between ac4C and chromatin modification, with the aim of advancing NAT10-based precision oncology.
