The Chinese Society of Hepatology of the Chinese Medical Association has invited experts in relevant fields to revise and rename the 2019 “Chinese Guidelines on the Management of Liver Cirrhosis” to “Chinese Guidelines for Clinical Diagnosis, Treatment, and Management of Cirrhosis (2025)”. These updated guidelines are aimed at providing recommendations for the clinical diagnosis and management of liver cirrhosis across the compensated, decompensated, and recompensated stages, as well as guidance on cirrhosis reversal and associated complications.

Craniopharyngioma (CP), although histologically benign, is a surgically challenging sellar-region tumor for which stereotactic irradiation is increasingly used as an alternative or adjuvant strategy. This review summarizes the role of stereotactic radiosurgery (SRS) in managing CP, with a focus on treatment outcomes, technical advances, and emerging strategies to support evidence-based clinical practice. Literature reports indicate that Gamma Knife radiosurgery achieves variable tumor control rates (36–100%), with optimal outcomes (79.6–91.4%) when marginal doses ≥12 Gy are delivered and patients receive adequate follow-up. Smaller tumors (<5 cm3) and those with higher solid components show particularly favorable outcomes. SRS demonstrates a favorable safety profile, with visual impairment occurring in approximately 4% of cases and endocrine dysfunction in 6%. Compared to conventional radiotherapy, SRS significantly reduces the risk of hypothalamic obesity in pediatric patients. The identification of BRAF mutations in papillary CPs has created novel opportunities for combining targeted therapies with SRS. Collectively, these advances underscore the role of SRS as an essential component of multidisciplinary CP management, particularly in the treatment of residual or recurrent lesions. It offers a more favorable toxicity profile and may improve quality of life outcomes compared to conventional radiotherapy. Further studies are needed to optimize patient selection, dosing strategies, and integration with novel systemic therapies.

Aging is characterized by a progressive decline in physiological function, an increased risk of chronic diseases, and multiple molecular and cellular alterations, including inflammation, oxidative stress, and mitochondrial dysfunction. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), initially developed for the treatment of type 2 diabetes and obesity, may modulate pathways associated with the hallmarks of aging. This review aims to summarize the mechanistic and therapeutic evidence for GLP-1 RAs in targeting key aging processes and their potential to restore cellular homeostasis and enhance healthspan. A comprehensive literature search was conducted in PubMed, Scopus, and Web of Science up to August 2025. Both preclinical and clinical studies were included if they evaluated the effects of GLP-1 RAs on the major biological processes encompassed by the 12 hallmarks of aging, such as mitochondrial dysfunction, insulin resistance, dysbiosis, inflammaging, autophagy, proteostasis, and genomic stability. Data were analyzed narratively to elucidate potential mechanisms and translational relevance. Evidence from animal and human studies demonstrates that GLP-1 RAs improve mitochondrial function, reduce oxidative stress, attenuate chronic inflammation, and enhance autophagic activity. Additionally, they modulate nutrient-sensing pathways and metabolic processes, thereby improving cellular resilience. Preclinical studies indicate neuroprotective, cardioprotective, and hepatoprotective effects, while emerging clinical data support improvements in metabolic and inflammatory profiles in older adults. Taken together, GLP-1 RAs exert pleiotropic effects across all 12 hallmarks of aging. Although long-term safety and efficacy require further evaluation, current evidence positions GLP-1 RAs as promising therapeutic agents in translational geroscience, with the potential to mitigate age-related physiological decline and promote a longer, healthier lifespan.

The advent of nanoparticle technology has transformed oncology therapeutics through its capacity for accurate drug delivery and regulated pharmaceutical release, boosting treatment effectiveness while minimizing adverse reactions. Various nanostructures, including polymeric carriers, liposomal formulations, and metal-based nanoparticles, can be engineered with tumor-specific targeting molecules to facilitate cellular uptake in malignant cells. Despite these advancements, issues such as production scalability, potential chronic toxicity, and regulatory approval processes still need to be addressed. Viral nanoparticles and virus-like particles (VLPs) represent innovative tools in nanotechnology and biomedicine, offering exceptional potential for targeted therapies, immune modulation, and diagnostic applications. Their natural biocompatibility, precise structural organization, and capacity for surface modification make them highly suitable for developing strategies to treat malignant tumors. Alongside VLP development, other approaches have also been investigated, such as magnetic hyperthermia, where magnetic nanoparticles are used to generate localized heat under an external magnetic field, selectively destroying cancer cells while sparing healthy tissue. This paper presents a brief review of nanocarriers in drug delivery systems and discusses the integration of nanoparticles, viral nanoparticles, and VLPs. Additionally, we explore the challenges and propose cutting-edge solutions, offering a forward-looking perspective on how the combination of these advanced technologies could transform oncology.

Autoimmune hepatitis (AIH) is an inflammatory liver disease influenced by genetic, environmental, and immunologic factors. Individuals diagnosed with AIH may exhibit concurrent autoimmune manifestations affecting multiple organ systems. The prevalence of AIH associated with other autoimmune diseases has been reported to range from 20% to 40%. This review indicates that the associations between AIH and autoimmune thyroiditis, type 1 diabetes mellitus, ulcerative colitis, Crohn disease, and celiac disease appear to be significant. However, the associations between AIH and primary sclerosing cholangitis, primary biliary cholangitis, rheumatoid arthritis, systemic lupus erythematosus, Sjögren syndrome, and vitiligo are not well-supported. The aim of this review is to evaluate the strength of the reported associations between AIH and other autoimmune diseases, and to update and present the available evidence on their prevalence, proposed underlying pathogenic mechanisms, diagnostic considerations, and treatment approaches.

Primary biliary cholangitis (PBC) is a chronic progressive autoimmune disorder characterized by small non-purulent intrahepatic bile duct destruction (ductopenia) and cholestasis. While the etiology of PBC remains unclear, it is believed to involve genetic-environmental interactions. Emerging evidence highlights gut microbiota dysbiosis in PBC patients, with increased symbiotic bacteria and decreased pathogenic bacteria. Microbial alterations potentially influence disease pathogenesis through multiple mechanisms, including immune dysregulation, intestinal barrier damage, BA metabolic dysregulation, and cholestasis. These findings suggest that the gut microbiota can serve not only as a non-invasive biomarker for diagnosis and prognosis evaluation but also as a therapeutic target for the disease. In this review, we summarize changes in PBC patients’ gut microbiota, explain how these changes affect disease occurrence and development, and discuss treatment methods with potential clinical value that intervene in gut microbiota.

Targeted drug delivery remains a major challenge in cancer therapy, often limiting both efficacy and safety. Although microRNA sponges and short-hairpin RNAs show potential for gene-based cancer treatment, their clinical use is restricted by delivery inefficiency, off-target effects, cytotoxicity, and instability. Viral vectors offer high efficiency but are associated with issues such as immune responses, insertional mutagenesis, and limited cargo capacity. Non-viral carriers are safer and more affordable but suffer from poor transfection efficiency, instability, and inadequate endosomal escape. These limitations hinder the clinical application of RNA therapeutics. The Vir-inspired Biotechnical Vector (VIBV) is a novel hybrid platform that combines viral and non-viral elements with nanotechnology to enable personalized, tumor-specific gene therapy. Engineered with a spindle-shaped nanocore and a polyethylene glycolylated liposomal shell, VIBV ensures immune evasion, prolonged circulation, and controlled therapeutic release triggered by tumor microenvironmental cues such as acidity, hypoxia, and elevated glutathione levels. It delivers oncogenic microRNA sponges, short-hairpin RNAs, tumor-specific antigens, and cyclin-targeting RNAs to enhance gene silencing, immune activation, and tumor suppression. This review examines the limitations of current delivery systems and presents VIBV as a promising next-generation strategy with improved biocompatibility, targeting precision, and potential for cost-effective, personalized cancer therapy, while also addressing its remaining challenges and prospects.

Hepatocellular carcinoma (HCC) is the most common subtype of primary liver cancer and continues to be a major cause of cancer-related mortality, particularly in regions of China with a high hepatitis B virus prevalence. Early-stage diagnosis remains challenging due to its asymptomatic onset and the limited sensitivity of conventional biomarkers, which together contribute to delayed detection, suboptimal therapeutic outcomes, and poor prognosis. These limitations underscore the urgent need for reliable, sensitive, and specific biomarkers to enable timely detection and targeted intervention. Protein induced by vitamin K absence or antagonist-II, an abnormal prothrombin variant generated under vitamin K deficiency or antagonism, has emerged as a promising candidate with diagnostic and therapeutic relevance in HCC. This review critically examines the molecular and biological characteristics of protein induced by vitamin K absence or antagonist-II, evaluates its clinical utility in HCC diagnosis and management, and delineates the current limitations hindering its broader application. Furthermore, future perspectives are proposed to guide translational research and clinical implementation. Collectively, this review aims to provide a comprehensive theoretical framework to advance precision diagnosis and individualized treatment strategies for HCC.

Congenital portosystemic shunts (CPSS) are rare vascular anomalies characterized by abnormal communication between the portal and systemic venous systems, resulting in partial or complete diversion of portal blood away from the liver. These shunts can give rise to a broad spectrum of clinical manifestations, including hyperammonemia (with or without encephalopathy), hepatopulmonary syndrome, and portopulmonary hypertension. Notably, these complications often occur in the absence of portal hypertension. Advances in diagnostic imaging, particularly Doppler ultrasound, computed tomographic angiography, and magnetic resonance imaging, have enhanced the early detection and classification of CPSS. Treatment approaches vary depending on shunt type and clinical severity and may include interventional closure via embolization or surgical ligation. Most persistent or symptomatic shunts require immediate intervention. Recent studies have also identified potential genetic and embryological mechanisms contributing to CPSS development, offering new insights into their pathogenesis. This review aims to summarize current knowledge on the epidemiology, pathophysiology, clinical presentation, diagnostic evaluation, and management of CPSS, and to highlight their consideration in patients with hepatic encephalopathy or unexplained liver disease.

Familial hypobetalipoproteinemia (FHBL), caused by apolipoprotein B (APOB) variants, disrupts APOB-containing lipoprotein synthesis, leading to reduced serum total cholesterol, low-density lipoprotein cholesterol, and APOB. Heterozygous carriers are often asymptomatic, while homozygotes exhibit severe manifestations like malabsorption, vitamin deficiencies, and hepatic steatosis. In recent years, FHBL has attracted increasing attention due to its association with liver disease and its role as a unique monogenic model of steatotic liver disease independent of cardiometabolic risk factors. Mechanistically, lipid overload, endoplasmic reticulum stress, oxidative damage, and impaired autophagy may drive hepatocellular injury and fibrosis. Challenges include insufficient diagnosis, sparse epidemiological data, and unclear disease progression. Enhanced genetic testing, mechanistic research, and longitudinal studies are critical to improving diagnosis, risk assessment, and therapies for FHBL-associated liver disease.