Metabolic dysfunction-associated fatty liver disease （MAFLD） is a chronic liver condition closely associated with dysregulated lipid metabolism，with the central pathological event of mitochondrial dysfunction in hepatocytes. The mitochondrial calcium uniporter （MCU） complex is a key molecular apparatus regulating mitochondrial calcium （mtCa²⁺） homeostasis，and mtCa²⁺ overload due to its dysfunction plays a critical role in the progression of MAFLD. This article systematically elaborates on the pathogenesis of MAFLD，with a particular focus on how the central signaling axis of “MCU complex dysfunction-mtCa²⁺ overload” drives the disease progression of MAFLD by disrupting energy metabolism，activating the adenosine monophosphate-activated protein kinase signaling pathway，triggering the NOD-like receptor protein 3 inflammasome，and inducing cell death. It also points out that traditional Chinese medicine can exert an interventional effect on multiple downstream pathways through various targets and has shown unique advantages and a significant potential in alleviating MAFLD by maintaining mitochondrial homeostasis and targeting the MCU complex，and therefore，it is expected to provide new strategies for the prevention and treatment of MAFLD.

Metabolic dysfunction-associated fatty liver disease （MAFLD） is the most prevalent chronic liver disease worldwide，with a complex pathogenesis. Mitochondria play a pivotal role in this disease process，and studies have confirmed that mitochondrial dysfunction can exacerbate metabolic disorders and induce innate immune imbalance，while mitochondrial DNA （mtDNA） is the core molecule mediating these two pathological effects. After the abnormal release of mtDNA，it can be recognized by intracellular pattern recognition receptors，which in turn triggers innate immune responses and causes tissue damage，forming a pathological pathway of “mtDNA release-immune activation-tissue damage”. Currently，there is a lack of systematic reviews summarizing the mechanism of action of this pathway in different stages of MAFLD and the intervention strategies targeting this pathway. This article systematically reviews the core molecular mechanism of this pathway，its pathological role in the development and progression of MAFLD，and the current intervention strategies targeting this mechanism，in order to provide a theoretical basis for analyzing the pathogenesis of MAFLD and developing novel therapeutic strategies.

Metabolic dysfunction-associated fatty liver disease （MAFLD） progresses to metabolic dysfunction-associated steatohepatitis （MASH） due to mitochondrial homeostasis imbalance and dysfunction in hepatocytes caused by various factors such as lipotoxicity and inflammatory infiltration. Recent studies have confirmed that mitochondrial injury is closely associated with chronic inflammation，with extracellular vesicle （EV） acting as a key mediator linking the two processes. This article systematically reviews the molecular mechanisms of hepatocyte mitochondrial dysfunction in MAFLD/MASH，highlights the regulatory role of hepatocyte-derived EV in intrahepatic inflammation，and discusses the potential application prospects of mitochondria-targeted therapies and intercellular communication interventions in MAFLD/MASH，in order to provide a theoretical basis for developing novel therapeutic strategies for these diseases.

Patients with craniopharyngioma are at a high risk of developing metabolic dysfunction-associated fatty liver disease and its severe complications，yet this association is often neglected in clinical practice，with a lack of systematic reviews. This article systematically reviews the clinical spectrum and epidemiological characteristics of liver diseases associated with craniopharyngioma，with a focus on their core pathogenic mechanisms，and it also summarizes current tumor treatment strategies aimed at preventing hypothalamic injury and highlights that establishing a multidisciplinary collaborative diagnosis and treatment model and implementing early intervention are key to improving prognosis. Future research should focus on elucidating the precise pathways through which hypothalamic injury leads to metabolic disturbances，thereby facilitating the development of targeted therapies，in order to provide new directions for fundamentally improving the clinical outcomes of these patients.

Liver fibrosis is a key pathological process in the transition from chronic liver disease to cirrhosis，especially in elderly patients with chronic hepatitis B，and this process is characterized by rapid progression and poor prognosis. T cell function gradually declines with aging，and T cell senescence is recognized as a key immunological mechanism accelerating the progression of liver fibrosis. Current studies have shown that senescent T cells promote the transition from liver fibrosis to liver cirrhosis by altering the liver inflammatory microenvironment，modulating the activity of fibrosis-related cells，and impairing immune surveillance function. This article systematically reviews the molecular mechanisms of T cell senescence and its role in the progression of liver fibrosis in elderly patients with chronic hepatitis B，as well as novel therapeutic approaches targeting immunosenescence with reference to the latest immunological findings and stem cell-based therapeutic strategies，so as to provide theoretical support for precise intervention for such patients.

Liver injury due to acetaminophen overdose is one of the main causes of acute liver failure，with a complex pathogenesis. In this process，liver sinusoidal endothelial cell （LSEC） injury is a key early event jointly mediated by factors such as oxidative stress，cell apoptosis，and imbalance between fibrinolysis and coagulation. Subsequent LSEC dysfunction further induces sinusoidal microcirculatory disturbances，amplifies the inflammatory response，impairs the regeneration and repair abilities of the liver，and finally causes hepatocyte necrosis. This article systematically elaborates on the critical role and molecular mechanism of LSEC in acetaminophen-induced liver injury，in order to provide a theoretical basis for novel therapeutic strategies and research directions.

The pathogenesis of idiosyncratic drug-induced liver injury （IDILI） remains unclear due to the rarity and unpredictability of IDILI and a lack of effective in vitro and in vivo models. Recent studies have shown that human leukocyte antigen （HLA） gene polymorphisms are significantly associated with the susceptibility to IDILI induced by various drugs. This article systematically reviews the latest research advances in HLA gene testing for IDILI，with a focus on the association between specific HLA gene loci and genetic susceptibility to drug-induced liver injury caused by commonly used drugs，in order to highlight the significance of HLA gene testing in IDILI screening.

Mild cognitive impairment （MCI） is a critical precursor stage of Alzheimer’s disease，and the development of MCI is closely associated with liver function. As a core metabolic organ，the liver regulates cognitive function through the liver-brain axis. Epidemiological studies have shown the association between liver function parameters and MCI. The liver affects cognitive function by clearing peripheral β-amyloid （mainly via the PPARα-LRP-1 pathway），secreting hepatic factors such as FGF21 and sEH to modulate neuronal energy metabolism，and mediating oxidative stress and systemic inflammatory responses. Anti-inflammatory/antioxidant measures，dietary pattern adjustments，and aerobic exercise are currently effective strategies for regulating liver function and mitigating mild cognitive impairment. This article systematically reviews the role and mechanism of the liver-brain axis in MCI，in order to provide new perspectives for developing liver-targeted therapies for cognitive impairment.