Colorectal cancer (CRC) is presently a health challenge in China. Although clinical chemotherapy is prescribed availably, the negative effects and poor prognoses still occur. Genistein has antitumor properties in our previous studies. However, the molecular mechanisms underlying the anti-CRC effects of genistein remain unclear. Increasing evidences have indicated that the induction of autophagy, one of cell death models, is closely associated with the formation and development of human cancer. In the current study, a systematic bioinformatics approach using network pharmacology and molecular docking imitation was aimed at identifying the pharmacological targets and anti-CRC mechanisms of genistein, characterized by autophagy-related processes and pathways. Moreover, experimental validation was conducted by using clinical and cell culture samples. All 48 potential targets of genistein-anti-CRC-associated autophagy were screened accordingly. Further bioinformatics analyses identified 10 core genistein-anti-CRC targets related to autophagy, and enrichment-assayed results revealed that the biological processes of these core targets might regulate multiple molecular pathways, including the estrogen signaling pathway. Additionally, molecular docking data demonstrated that genistein has a high affinity for epidermal growth factor receptor (EGFR) and estrogen receptor 1 (ESR1). Both EGFR and ESR1 proteins were highly expressed in clinical CRC samples. Preliminary in vitro data showed that genistein effectively reduced cellular proliferation, activated apoptosis, and suppressed EGFR and ESR1 protein expressions in CRC cells. Our research findings uncovered the molecular mechanisms of genistein against CRC, and the potential drug targets associated with autophagy in genistein treatment of CRC were identified and validated experimentally, including EGFR and ESR1.

Objective: The aim of this study was to summarize the effects of amino acids (AA) on renal function and nutritional indices in patients with renal insufficiency (RI) after treatment and to analyze the development trend in this field. Methods: The bibliometric evaluation of scholarly contributions in this field was conducted using the Web of Science database, with data analyzed via Bibliometrix and VOSviewer software. The randomized controlled trials (RCTs) published before January 13, 2025, were systematically retrieved from Embase, PubMed, and the Cochrane Library and meta-analyses were performed using Review Manager 5.4 software. Results: Key areas of focus included oxidative stress, chronic renal failure, hemodialysis, inflammation, chronic kidney disease, risk, plasma, progression, L-arginine, disease, and renal failure. Nine RCTs involving 407 participants were included, AA administration demonstrated significant effects compared to placebo: Increased blood urea nitrogen (MD: 4.21, 95% CI: 1.08 to 7.35, p = 0.008), elevated renal plasma flow (MD: 30.78, 95% CI: 15.36 to 46.21, p < 0.0001), and reduced uric acid levels (MD: −0.47, 95% CI: −0.89 to −0.06, p = 0.02). Conclusion: These findings suggest that AA supplementation may partially improve renal function in RI patients. The progression and possible mechanisms of chronic kidney disease, as well as the search for new biomarkers, will be the trend of research and development in this field.

Background: The Global Leadership Initiative on Malnutrition (GLIM) criteria were officially introduced in 2018 with the aim of establishing a standardized global framework for the diagnosis of malnutrition. Synthesizing expert consensus from multiple international organizations, the GLIM criteria proposed a two-step diagnostic model integrating both phenotypic and etiologic components. Although GLIM-related research has expanded rapidly in recent years, a comprehensive bibliometric evaluation remains absent.Methods: Relevant literature published between 2018 and 2024 was retrieved from the Scopus database. Only English-language original research articles and reviews were included. A total of 729 eligible publications were analyzed using VOSviewer (v1.6.10), CiteSpace (v5.8.R3), and the online platform Bioinformatics. The analysis covered various dimensions, including countries, institutions, authors, journals, keywords, and highly cited references.Results: The volume of GLIM-related publications has shown a steady upward trajectory, peaking in 2024. China emerged as the most prolific country, followed by Spain and Japan. The top contributing institutions included Uppsala University, Capital Medical University, and Beijing Shijitan Hospital. Among the most productive authors were Cederholm T, Shi H, and Correia MITD. Clinical Nutrition and Nutrients were identified as the core journals in this field. Keyword analysis revealed that “malnutrition,” “diagnosis,” “sarcopenia,” “cancer,” and “nutritional risk” were pre-dominant themes, while “systematic review,” “protein blood level,” and “gastric cancer” represented emerging areas of interest.Conclusion: This study represents the first comprehensive bibliometric analysis of research related to the GLIM criteria. It identifies key contributors, collaboration networks, and thematic evolutions in the field, highlighting a transition from the development of diagnostic frameworks to clinical application and individualized nutritional assessment. These findings provide a valuable reference for guiding future research directions in GLIM-related domains.

The relationship between major depressive disorder (MDD) and liver diseases is complex, with causal links poorly understood. This study aimed to disentangle causal, mediated, and confounded links between MDD and liver diseases. We integrated three approaches: a trend analysis of 2004 to 2024 publications; a two-sample Mendelian randomization, or MR, analysis assessing genetic causal effects of MDD on liver diseases; and an observational analysis of the NHANES 2007 to 2020 cohort using survey-weighted regression and formal causal mediation analysis to evaluate clinical pathways. MR analysis provided genetic evidence for a causal effect of MDD on NAFLD (OR = 1.233, 95% CI: 1.015-1.496), chronic HBV (OR = 1.607, 95% CI: 1.155-2.235), and viral hepatitis (OR = 1.515, 95% CI: 1.053-2.180), but not chronic HCV. In NHANES, the clinical MDD-NAFLD association (AOR = 1.35) became non-significant after adjusting for BMI (AOR = 1.07, P = 0.500), with formal mediation analysis revealing that BMI significantly mediates 80.70% of this risk. Furthermore, MDD showed no independent association with advanced liver fibrosis (P = 0.500). Conversely, a strong observational association was found for chronic HCV (AOR = 2.52) despite the null MR finding; however, this was entirely attenuated after adjusting for illicit drug use (AOR = 1.59, P = 0.072). No significant association was found for chronic HBV. MDD increases liver disease risk via distinct pathways. The genetic MDD-NAFLD link appears largely mediated by obesity clinically, manifesting primarily as steatosis rather than direct fibrogenesis. The strong MDD-HCV association reflects socio-behavioral confounding, while the causal MDD-HBV link remains an under-recognized risk. These findings underscore the importance of managing obesity in psychiatric care and integrating mental health screening in hepatology.