Hepatobiliary & Pancreatic Diseases International最新文献

Background: Within the tumor microenvironment, survival pressures are prevalent with potent drivers of tumor progression, angiogenesis, and therapeutic resistance. N6-methyladenosine (m⁶A) methylation has been recognized as a critical post-transcriptional mechanism regulating various aspects of mRNA metabolism. Understanding the intricate interplay between survival pressures and m⁶A modification provides new insights into the molecular mechanisms underlying hepatocellular carcinoma (HCC) progression and highlights the potential for targeting the survival pressures-m⁶A axis in HCC diagnosis and treatment.

Data sources: A literature search was conducted in PubMed, MEDLINE, and Web of Science for relevant articles published up to April 2024. The keywords used for the search included hepatocellular carcinoma, cellular survival, survival pressure, N6-methyladenosine, tumor microenvironment, stress response, and hypoxia.

Results: This review delves into the multifaceted roles of survival pressures and m⁶A RNA methylation in HCC, highlighting how survival pressures modulate the m⁶A landscape, the impact of m⁶A modification on survival pressure-responsive gene expression, and the consequent effects on HCC cell survival, proliferation, metastasis, and resistance to treatment. Furthermore, we explored the therapeutic potential of targeting this crosstalk, proposing strategies that leverage the understanding of survival pressures and m⁶A RNA methylation mechanisms to develop novel, and more effective treatments for HCC.

Conclusions: The interplay between survival pressures and m⁶A RNA methylation emerges as a complex regulatory network that influences HCC pathogenesis and progression.

Background: Gallstone disease (GSD), nonalcoholic fatty liver disease (NAFLD), metabolic dysfunction-associated fatty liver disease (MAFLD), and metabolic syndrome (MetS) are common medical disorders worldwide. This study aimed to ascertain how NAFLD, MAFLD, MetS, and other factors affect the development of GSD, and how the GSD-associated factors influence patient recovery after laparoscopic cholecystectomy (LC).

Methods: We included 200 patients who were diagnosed with GSD and underwent LC between January 2017 and February 2022. A total of 200 subjects without GSD and "non-calculous causes" during the same period were also included as controls. We compared the metabolic disorder differences between GSD patients and controls. Furthermore, we sub-grouped patients based on the comorbidities of preoperative NAFLD, MAFLD, and MetS, and compared the impacts of these comorbidities on short-term post-LC functional recovery of the patients.

Results: The prevalence of NAFLD and MetS were higher in GSD patients (P < 0.05). Based on multivariate logistic regression analysis, hyperglycemia [odds ratio (OR) = 2.2, 95% confidence interval (CI): 1.4-3.4, P = 0.001] and low high-density lipoprotein cholesterol (HDL-C) level (OR = 1.8, 95% CI: 1.1-3.1, P = 0.048) were linked to GSD. NAFLD and MetS linked to liver enzymes after LC (P < 0.05). MetS also linked to the levels of inflammatory indicators after LC (P < 0.05). The obesity, hyperlipidemia, low HDL-C level, and hyperglycemia linked to liver enzymes after LC (P < 0.05). Hyperlipidemia, low HDL-C level, and hypertension linked to inflammation after LC (P < 0.05).

Conclusions: The prevalence of GSD may be linked to NAFLD and MetS. Hyperglycemia and low HDL-C level were independent risk factors of GSD.