High-mobility group box-1 (HMGB1) is an architectural chromosomal protein with various roles depending on its cellular localization. Extracellular HMGB1 functions as a prototypical damage-associated molecular pattern that triggers inflammation and adaptive immune responses, mediated by specific cell surface receptors, including receptors for advanced glycation end products and toll-like receptors. Post-translational modifications of HMGB1 significantly impact various cellular processes that contribute to the pathogenesis of liver diseases. Recent studies have highlighted the close relationship between HMGB1 and the pathogenesis of acute liver injuries, including acetaminophen-induced liver injury, hepatic ischemia-reperfusion injury, and acute liver failure. In chronic liver diseases, HMGB1 plays a role in nonalcoholic fatty liver disease, alcohol-associated liver disease, liver fibrosis, and hepatocellular carcinoma. Targeting HMGB1 as a therapeutic approach, either by inhibiting its release or blocking its extracellular function, is a promising strategy for treating liver diseases. This review aimed to summarize the available evidence on HMGB1’s role in liver disease, focusing on its multifaceted signaling pathways, impact on disease progression, and the translation of these findings into clinical interventions.

Drug-induced liver injury (DILI) is a harmful reaction to medications, herbs, and dietary supplements that results in liver dysfunction. Based on the distinct clinical patterns of liver damage, DILI can be categorized into hepatocellular, cholestatic, and mixed types. Hepatocellular DILI is linked to inflammation, apoptosis, and necrosis, while cholestatic DILI is commonly associated with bile plugs and, in rare cases, ductopenia. Ursodeoxycholic acid (UDCA) is the therapeutic agent most widely used for the treatment of cholestatic hepatopathies of diverse etiologies and has been mainly used as a supportive treatment in cholestatic DILI. In this review, we presented a more structured and systematic framework for the potential application of this hepatoprotective agent across a broader range of DILI scenarios. A MEDLINE search of the literature from 1995 to the present retrieved 41 preliminary clinical studies suggesting that UDCA may offer curative and preventive benefits for hepatocellular DILI as well. This aligns with preclinical studies in rodents, showing beneficial effects of UDCA in experimental DILI irrespective of the clinical patterns of injury involved. This could be due to the broad range of potentially beneficial effects of UDCA, which may address the various types of liver damage with different causes and mechanisms seen in all forms of DILI. UDCA’s beneficial properties include anticholestatic, antioxidant, anti-inflammatory, anti-apoptotic, anti-necrotic, mitochondrial protective, endoplasmic reticulum stress-relieving, and immunomodulatory effects. Controlled studies with systematic use of standardized causality assessments are eagerly awaited to properly validate the use of UDCA in DILI. Meanwhile, we hope this article helps clarify and systematize the use of this versatile and safe hepatoprotective medication for different types of liver toxicity.

China has made remarkable progress in controlling chronic hepatitis B virus (HBV) infection over the past three decades. The prevalence of hepatitis B surface antigen has declined from 9.72% in 1992 to 5.86% in 2020, with a striking reduction from 9.67% to 0.30% among children under five. Universal hepatitis B vaccination has been pivotal, preventing more than 40 million infections and seven million HBV-related deaths since 1992. Nevertheless, an estimated 75 million individuals are currently living with chronic HBV infection in China. Among them, only 59.78% are aware of their infection status, and about 30 million remain undiagnosed. Of those diagnosed, 38.25% (approximately 17 million) meet the criteria for antiviral treatment, yet only 17.33% (about three million) are receiving treatment. To accelerate progress toward the World Health Organization’s elimination targets, China has updated its clinical guidelines to expand treatment eligibility and improve diagnosis and treatment coverage. Moreover, Chinese pharmaceutical companies and academic institutions are actively engaged in developing novel therapies with promising efficacy, aiming to achieve a functional cure. China’s holistic approach, combining evidence-based public health interventions with active clinical management and innovative pharmaceutical development, provides valuable experience for global HBV elimination initiatives. This review aimed to summarize China's progress in HBV control, identify remaining gaps in diagnosis and treatment, and highlight strategic approaches, including public health interventions, clinical policy updates, and pharmaceutical innovation, toward achieving HBV elimination.

Colorectal cancer (CRC) is the second most commonly diagnosed cancer in China. Early detection and diagnosis of CRC are essential for improving survival rates. However, socioeconomic factors such as regional disparities, economic conditions, and varying levels of awareness impact the uptake of screening programs. Recently, rapid advancements in non-invasive tests, including high-quality fecal immunochemical tests and the emergence of stool and blood biomarkers for CRC, have facilitated improvements in early detection and diagnosis. Additionally, image-enhanced endoscopy, a group of advanced imaging technologies, has been developed to assist in the early identification of colorectal lesions, including narrow band imaging and linked-color imaging. The emergence of artificial intelligence also offers promising opportunities to improve early diagnosis and treatment of CRC. This review mainly introduces screening technologies and the current status of CRC screening in China, provides an overview of CRC early detection and diagnosis, and discusses the limitations and future prospects.

Inflammatory bowel disease (IBD) is an idiopathic intestinal inflammatory condition affecting the ileum, colon, and rectum, including ulcerative colitis and Crohn’s disease. Clinical symptoms include abdominal pain, diarrhea, and even bloody stools. The intestinal barrier is the first line of defense between the intestinal tract and the external environment, and maintaining its stability is essential for intestinal health. On one hand, it enables the digestion and absorption of water and nutrients; on the other, it plays a crucial role in reducing the absorption of toxins and the invasion of pathogens. Damage to the intestinal barrier has become one of the most important factors in the onset and progression of IBD. However, there is currently no literature that systematically reviews the mechanisms of the intestinal barrier in the pathogenesis of IBD and the factors influencing it. In this paper, we aimed to systematically elaborate on the role of the intestinal barrier in IBD through the perspectives of oxidative stress, intestinal flora, and cellular autophagy. Our goal was to explore the mechanisms of the intestinal barrier in IBD more deeply and to provide new insights for the diagnosis and treatment of IBD. This article will summarize the composition of the intestinal barrier, the factors affecting it, and strategies to protect it.

Memory loss is a symptom of several neurological disorders, including dementia and Alzheimer’s disease (AD). It can significantly impact individuals, their loved ones, and society as a whole. Current pharmaceutical interventions have shown some improvement in individuals’ quality of life, but more needs to be done to reduce the burden of memory loss and AD. This paper investigates herbal remedies for memory loss, with a particular focus on the mechanisms underlying their effects. By consulting several South Asian printed books, numerous traditionally used medicinal plants with memory-enhancing properties were identified. A review of published studies showed that many of these plants have reported properties related to memory enhancement and the treatment of AD. Some of the relevant mechanistic actions reported for these plants include acetylcholinesterase inhibition, anti-inflammatory activity, antioxidant effects, and neuroprotective properties. There is also evidence that some plants exhibit a combination of different mechanisms, making them especially promising as therapeutic agents for memory loss. Our review shows the existence and potential of medicinal plants in addressing memory loss. Additionally, some reports provide a scientific basis for the use of these plants in conditions characterized by memory decline, such as AD. This study underscores the importance of further research to evaluate the efficacy of traditionally used medicinal plants in the management of memory loss.

Free radicals are produced in the body during normal cellular metabolic activities, and their excessive accumulation can overwhelm the natural antioxidant mechanisms. This leads to oxidative stress, which is associated with the development and progression of non-communicable diseases (NCDs) such as liver and kidney diseases, cardiovascular diseases, neurodegenerative diseases, cancer, and diabetes. Enzymes play a significant role in maintaining a balance between antioxidants and free radicals by either enhancing the production of antioxidants or slowing down the generation of free radicals in the body. There is no up-to-date review on how antioxidant-enzyme interactions modulate the development and progression of NCDs. This review, therefore, discusses the mechanisms of antioxidant-enzyme interactions in the control of oxidative stress, as well as the implications and prospects of these interactions in the management of NCDs. Therapeutic strategies targeting antioxidant-enzyme interactions in the natural defense mechanisms of the body against oxidative stress can provide targeted benefits in the management of various NCDs. The mechanisms of interaction of some antioxidants with catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase, glutathione S-transferases, thioredoxin protein, and thioredoxin reductase suggest their strong involvement in mitigating the development and progression of NCDs. Moreover, understanding the specific interactions and signaling pathways involved in antioxidant-enzyme interactions could facilitate the emergence of novel and effective therapeutic strategies for the management of NCDs and should be considered a primary goal of future studies. This study provides the necessary template, encourages discussion, and creates more opportunities for the next stage in the development of antioxidant therapies.

Pancreatic ductal adenocarcinoma (PDAC) is an aggressive disease with difficulties in early diagnosis, poor prognosis, and limited effective therapies. Early detection and effective treatment offer the optimal chance to improve survival rates. Various studies have shown that gut microbiota dysbiosis is closely related to PDAC, with potential mechanism involving immune regulation, metabolic process impact, and reshaping the tumor microenvironment. A comprehensive understanding of the microbiota in PDAC might lead to the establishment of screening or early-stage diagnosis methods, implementation of cancer bacteriotherapy such as fecal microbiota transplantation, creating new opportunities and fostering hope for desperate PDAC patients.

Metabolic dysfunction-associated steatotic liver disease has emerged as a leading cause of chronic liver disease and cirrhosis in the Western world. With rising rates of obesity, the prevalence of metabolic dysfunction-associated steatohepatitis (MASH)-related cirrhosis is expected to increase. MASH is associated with chronic hepatic inflammation and progressive liver fibrosis, and significant research is focused on developing pharmacological therapies to reverse these downstream complications. Recent trials have explored various therapeutic targets across metabolic, inflammatory, and fibrogenic pathways aimed at decreasing liver triglycerides, inflammation, lipotoxicity, and fibrosis. Some of these drugs show promise in reversing biomarkers and/or histologic markers of steatohepatitis and fibrosis, although most have been primarily studied in non-cirrhotic patients. However, in the context of the significant unmet medical need of patients with MASH-associated cirrhosis, growing interest in targeting compensated cirrhosis has prompted renewed investment in numerous early clinical and late-stage programs evaluating novel investigational agents in this population. This review summarizes current therapies under evaluation in phase 2 and 3 clinical trials for MASH-related cirrhosis, highlighting drug mechanisms, outcomes, and future research directions.