Hepatic encephalopathy and other neurodegenerative disorders have profound implications for extensive liver impairment, calling for new ways of treating the condition. The application of stem cell transplantation to treat these severe disorders is a new and encouraging technique. This review article digs deep into the subject of stem cell transplantation therapy, neurodegenerative disorders associated with advanced liver damage, and liver transplantation. It comprehensively analyses the background, rationale, scope, and objectives of using stem cells to treat such challenging conditions. The topic of discussion includes the subtleties of neurodegenerative disorders, the function of liver transplantation, and the possible advantages and disadvantages associated with it. The relevance of patient selection, intraoperative concerns and post-transplant care is discussed. Further, the article explores how stem cell-based therapies can benefit from nanotechnology, specifically how it can improve stem cell distribution, survival, and integration for better therapeutic results. This review aims to offer a thorough analysis of regenerative medicine’s present and future possibilities in dealing with the intricate relationship between neurodegeneration and liver damage. It does this by examining the efficacy, safety, and long-term impacts of stem cell transplantation in treating neurodegenerative disorders associated with advanced liver damage. This will incorporate insights from ongoing clinical trials, the patent landscape, and future directions. The goal is to pave the way for innovative and personalized treatment approaches in this evolving research and clinical practice field. Therefore, these efforts represent a promising frontier in medical research that can alleviate the burden of HE and associated neurological complications combined with liver cirrhosis.

Background: Portal cavernoma, a complex vascular disease characterized by the formation of a branch structure because of portal vein thrombosis, remains a significant clinical concern. This study explores the current understanding of the molecular mechanism, including dysregulation of angiogenesis signaling, immunological chain reactions and impaired endothelial function for cavernoma development. Objective: There is no FDA-approved specific drug for portal vein complications. Hence objective of this review is to maximize treatment and enhance patient outcomes, by a collaborative effort, comprising gastrointestinal specialists, interventional radiologists and hepatobiliary surgeons to improve long-term results and quality of life for these patients. Methods: Drug therapies aimed at VEGF, or TGF-β, along with hypoxia-inducible elements, exhibit potential to manage portal cavernoma. Current biological findings have uncovered new pathways driving their origins, resulting in possible drug targets and novel treatment techniques. Growing approaches to treatment, mainly anti-angiogenic medications, focused on genetic therapy and immune system modulation, suggest the potential in addition to conventional blood coagulation, along with surgical techniques. Results: Current treatment strategies frequently rely on case reports that lack defined treatment standards. Long-term outcomes of various therapeutic techniques, optimal anticoagulation strategies and the involvement of endovascular or surgical therapies are all important areas that require additional research. Despite the serious clinical implications, portal cavernoma remains underrepresented in the literature. Conclusion: This review highlighted the requirement for necessary clinical understanding for management and further investigation into this complex disorder and also covers the gaps in understanding molecular mechanisms, utilizing standardized therapeutic strategies and focusing on individualized treatment plans for patients of portal cavernoma.