Core fucosylation, catalyzed exclusively by fucosyltransferase 8 (FUT8), is an evolutionarily conserved post-translational modification that has emerged as a central regulatory hub linking liver homeostasis, chronic disease progression, and malignant transformation. Liver diseases, particularly hepatocellular carcinoma, remain a leading global health burden characterized by late diagnosis, limited therapeutic options, and poor overall survival. While aberrant glycosylation is now recognized as a hallmark of cancer and inflammatory disorders, existing research on FUT8-mediated core fucosylation in liver diseases remains fragmented: the dynamic functional switch of FUT8 from a homeostatic regulator to a pathological driver across the full disease continuum has not been systematically delineated, and the integrated mechanisms by which core fucosylation modulates oncogenic signaling, metabolic reprogramming, and immune evasion remain poorly understood. This review synthesizes recent advances to establish a unified framework for understanding the dual role of core fucosylation in liver physiology and pathology, and evaluates its translational potential for precision medicine. At the molecular level, FUT8’s unique catalytic specificity makes core fucosylation an irreplaceable modification, as evidenced by the perinatal lethality and severe organ dysfunction in Fut8 knockout mice. In hepatocellular carcinoma, genomic amplification of guanosine 5'-diphosphate-fucose biosynthetic enzymes provides metabolic support for aberrant core fucosylation. FUT8 expression is tightly regulated by a multi-layered network: transcriptional activation via Wnt/β‑catenin and wild-type p53, epigenetic upregulation by lncRNAs, post-transcriptional repression by miR-122-5p and miR-34a, and virus-specific induction by hepatitis B virus/hepatitis C virus. Physiologically, core fucosylation maintains liver homeostasis through four core mechanisms: it acts as a molecular switch for epidermal growth factor receptor/hepatocyte growth factor receptor signaling to enable liver regeneration; directs polarized secretion of hepatocyte-derived glycoproteins into bile ducts; modulates cholesterol metabolism via the hepatocyte nuclear factor 1α-proprotein convertase subtilisin/kexin type 9-low density lipoprotein receptor axis; and regulates aging through insulin‑like growth factor 1 receptor signaling. Pathologically, core fucosylation exhibits context-dependent dual functions: in liver fibrosis, FUT8 upregulation in hepatic stellate cells forms a negative feedback loop that limits excessive fibrogenesis; in hepatocellular carcinoma, however, aberrant FUT8 overexpression drives cell-autonomous malignancy by constitutively activating epidermal growth factor/hepatocyte growth factor receptor, transforming growth factor‑β/Smad, and Wnt/β‑catenin pathways, while simultaneously establishing a multi-layered immune evasion network by stabilizing programmed cell death ligand 1 and cluster of differentiation 47, and impairing natural killer cell homeostasis via interleukin‑2 receptor β glycosylation. Clinically, stage-specific core fucosylation biomarkers enable non-invasive monitoring of liver disease progression: low molecular mass kringle-Fc fusion protein outperforms conventional markers for early fibrosis detection, while alpha-fetoprotein-L3 and novel glycopeptides (α‑2‑macroglobulin N‑linked glycosylation site 1424, lumican core fucosylated peptide) significantly improve early hepatocellular carcinoma diagnosis, especially in alpha-fetoprotein-negative patients. Next-generation detection technologies (chemoenzymatic labeling, site-specific mass spectrometry) overcome the specificity limitations of traditional lectin assays. Therapeutically, four promising strategies are emerging: small-molecule FUT8 inhibitors, afucosylated antibodies with enhanced antibody‑dependent cellular cytotoxicity, Fuc-modified targeted drug delivery systems, and core fucose-specific lectins for NASH treatment. The core challenge for clinical translation lies in FUT8’s inherent “double-edged sword” effect, as systemic inhibition disrupts its essential physiological functions beyond pathological roles. Long-term systemic FUT8 blockade not only impairs post-injury liver regeneration by abrogating epidermal growth factor/hepatocyte growth factor receptor signaling but also disrupts cholesterol homeostasis via the hepatocyte nuclear factor 1α-proprotein convertase subtilisin/kexin type 9-low density lipoprotein receptor axis, leading to dyslipidemia and altered bile secretion. Critically, it compromises immune surveillance by destabilizing interleukin‑2 receptor β on natural killer cells, reducing their cytotoxic activity against malignant and virally infected cells, and impairs IgG Fc-mediated effector functions, increasing susceptibility to infections. This fundamental trade-off between therapeutic efficacy and systemic toxicity necessitates a paradigm shift from non-specific global inhibition to precision modulation of pathological core fucosylation. By addressing these critical challenges, FUT8-mediated core fucosylation has the potential to transform liver disease management from late-stage intervention to early detection and precision therapy, ultimately improving patient outcomes and reducing the global burden of liver diseases.

Numerous studies have shown that depression is main-ly associated with the abnormal expression of connexin 43(Cx43)in astrocytes(Astro)and its mediated dysfunction of gap junction(GJ).However,the molecular mechanism of post-translational modifications targeting Cx43 to regulate neuroin-flammation-associated depression is still unclear.Post-transla-tional modifications of Cx43 mainly include phosphorylation of specific amino acid sites by PKC,PKA,PKG,MAPK and PTK,and protein degradation of Cx43 through the K48/K63 polyubiq-uitylation and deubiquitination pathways,which ultimately lead to protein degradation through K48/K63 polyubiquitination and deubiquitination.These modifications are ultimately involved in the regulation of neuroinflammatory responses through the associ-ation of GJ function.In this paper,we systematically review the role of Cx43 post-translational modifications in neuroinflamma-tion,with the aim of further exploring the potential application of targeting these modifications to modulate the inflammatory re-sponse mechanism in improving depressive symptoms.

Chronic kidney disease(CKD)is a chronic disease characterized by renal structural damage and dysfunction.At present,there is still a lack of effective therapeutic drugs and prevention and treatment methods for CKD in clinical practice.More and more studies have shown that necroptosis,as a new type of programmed cell death,plays a vital role in the onset and progression of CKD.Targeting key molecules in the necroptosis pathway,such as RIPK1,RIPK3 and MLKL,the development of small molecule inhibitors has become an emerging strategy for the treatment of CKD,and has shown significant potential to pro-tect the kidneys and alleviate renal fibrosis in a variety of in vitro and in vivo models.Therefore,this article summarizes the re-search progress of the mechanism of necroptosis in recent years,and focuses on the potential role of necroptosis in the pathogene-sis of CKD and the therapeutic potential of targeting this path-way,providing a new perspective and research direction for the prevention and treatment of CKD in the future.

Objective This study aims to compare the clinical efficacy and complications associated with microwave ablation(MWA)and sublobectomyfor treating stage ⅠA non-small cell lung cancer(NSCLC).Methods Data from stage ⅠA1-ⅠA3 NSCLC patients treated at Yunnan Cancer Hospital between January 2021 and December 2022 were retrospectively collected.A total of 82 patients who underwent MWA and 82 patients who received sublobectomy were selected through propensity score matching.Periprocedural conditions,short-term efficacy,and complications were compared between the two groups.Progression-free survival(PFS)and Disease-free survival(DFS)were monitored and evaluated.The Kaplan-Meier method was employed to construct survival curves,and logistic regression was utilized to analyze the factors influencing complications.Results The MWA group exhibited shorter procedure times,less intraprocedural blood loss,less postprocedure pain,shorter hospitalization durations,and lower hospitalization costs compared to the sublobectomy group(P<0.001).All patients successfully underwent the procedures,with a complete ablation rate of 97.6%and a local control rate of 87.8%in the MWA group.The median follow-up duration was 26.5 months.Survival curve analysis indicated no statistically significant differences in PFS and DFS between the two groups.The primary complications observed were pneumothorax(24.4%,20/82)and moderate to severe pain(11.0%,9/82)in the MWA group,while the sublobectomy group experienced moderate to severe pain(41.5%,34/82)and pulmonary infection(12.2%,10/82).Single-factor analysis demonstrated six variables influenced the occurrence of MWA pneumothorax.Multi-factor logistic regression revealed that the shortest distance from the tumor to the pleura(P=0.021,OR=15.341,95%CI:1.699～24.367)and the number of punctures through the pleura(P=0.024,OR=0.068,95%CI:0.001～0.612)were identified as independent risk factors for pneumothorax.Conclusion MWA demonstrates good efficacy for treating stage ⅠA NSCLC due to minimal trauma,low cost,rapid recovery,few and mild complications.Additionally,MWA and sublobectomy exhibit comparable PFS and DFS,making MWA a safe and effective treatment method.Therefore,MWA is worthy of promotion in clini-cal practice.

Numerous studies have shown that depression is main-ly associated with the abnormal expression of connexin 43(Cx43)in astrocytes(Astro)and its mediated dysfunction of gap junction(GJ).However,the molecular mechanism of post-translational modifications targeting Cx43 to regulate neuroin-flammation-associated depression is still unclear.Post-transla-tional modifications of Cx43 mainly include phosphorylation of specific amino acid sites by PKC,PKA,PKG,MAPK and PTK,and protein degradation of Cx43 through the K48/K63 polyubiq-uitylation and deubiquitination pathways,which ultimately lead to protein degradation through K48/K63 polyubiquitination and deubiquitination.These modifications are ultimately involved in the regulation of neuroinflammatory responses through the associ-ation of GJ function.In this paper,we systematically review the role of Cx43 post-translational modifications in neuroinflamma-tion,with the aim of further exploring the potential application of targeting these modifications to modulate the inflammatory re-sponse mechanism in improving depressive symptoms.

Chronic kidney disease(CKD)is a chronic disease characterized by renal structural damage and dysfunction.At present,there is still a lack of effective therapeutic drugs and prevention and treatment methods for CKD in clinical practice.More and more studies have shown that necroptosis,as a new type of programmed cell death,plays a vital role in the onset and progression of CKD.Targeting key molecules in the necroptosis pathway,such as RIPK1,RIPK3 and MLKL,the development of small molecule inhibitors has become an emerging strategy for the treatment of CKD,and has shown significant potential to pro-tect the kidneys and alleviate renal fibrosis in a variety of in vitro and in vivo models.Therefore,this article summarizes the re-search progress of the mechanism of necroptosis in recent years,and focuses on the potential role of necroptosis in the pathogene-sis of CKD and the therapeutic potential of targeting this path-way,providing a new perspective and research direction for the prevention and treatment of CKD in the future.

Objective This study aims to compare the clinical efficacy and complications associated with microwave ablation(MWA)and sublobectomyfor treating stage ⅠA non-small cell lung cancer(NSCLC).Methods Data from stage ⅠA1-ⅠA3 NSCLC patients treated at Yunnan Cancer Hospital between January 2021 and December 2022 were retrospectively collected.A total of 82 patients who underwent MWA and 82 patients who received sublobectomy were selected through propensity score matching.Periprocedural conditions,short-term efficacy,and complications were compared between the two groups.Progression-free survival(PFS)and Disease-free survival(DFS)were monitored and evaluated.The Kaplan-Meier method was employed to construct survival curves,and logistic regression was utilized to analyze the factors influencing complications.Results The MWA group exhibited shorter procedure times,less intraprocedural blood loss,less postprocedure pain,shorter hospitalization durations,and lower hospitalization costs compared to the sublobectomy group(P<0.001).All patients successfully underwent the procedures,with a complete ablation rate of 97.6%and a local control rate of 87.8%in the MWA group.The median follow-up duration was 26.5 months.Survival curve analysis indicated no statistically significant differences in PFS and DFS between the two groups.The primary complications observed were pneumothorax(24.4%,20/82)and moderate to severe pain(11.0%,9/82)in the MWA group,while the sublobectomy group experienced moderate to severe pain(41.5%,34/82)and pulmonary infection(12.2%,10/82).Single-factor analysis demonstrated six variables influenced the occurrence of MWA pneumothorax.Multi-factor logistic regression revealed that the shortest distance from the tumor to the pleura(P=0.021,OR=15.341,95%CI:1.699～24.367)and the number of punctures through the pleura(P=0.024,OR=0.068,95%CI:0.001～0.612)were identified as independent risk factors for pneumothorax.Conclusion MWA demonstrates good efficacy for treating stage ⅠA NSCLC due to minimal trauma,low cost,rapid recovery,few and mild complications.Additionally,MWA and sublobectomy exhibit comparable PFS and DFS,making MWA a safe and effective treatment method.Therefore,MWA is worthy of promotion in clini-cal practice.

Aim To investigate the promotive effects and mechanisms of the combined use of brucine(Bru)and lumbrokinase(LK),active ingredient derived from Longma formula,in promoting chondrocyte proliferation via the Wnt/β-catenin signaling pathway.Methods The extracted primary rat chondrocytes were divided in-to the following groups:Control group,Bru,LK alone group,and Bro+LK combination group.The optimal drug concentration and intervention time were deter-mined using CCK-8 assay,followed by cell proliferation validation through EdU and phalloidin staining.The expression levels of collagen Ⅱ,aggrecan and SRY-re-lated high-mobility group box gene 9(SOX9)in chon-drocytes following intervention with the combination of Bru and LK were detected by Western blotting.Addi-tionally,the regulatory effects of these proteins on the Wnt/β-catenin signaling pathway were also investiga-ted.Results The optimal combination concentration of Longma formula active ingredients(Bru 0.025 mg·L-1+LK 5 mg·L-1)significantly enhanced chondro-cyte viability compared to control,Bru,or LK alone at 48 h.This combination increased the S-phase ratio,promoted the aggregation of intracellular actin fila-ments,and upregulated the expression of collagen Ⅱ and aggrecan.Furthermore,it activated the Wnt/β-catenin pathway,leading to increased SOX9 expres-sion.Conclusions The optimal combination of Bru and LK(Bru 0.025 mg·L-1+LK 5 mg·L-1)de-rived from Longma formula significantly maintains chondrocyte phenotype and promotes cellular prolifera-tion through the activation of the Wnt/β-catenin signa-ling pathway,which subsequently upregulates the downstream target SOX9.

Objective To investigate the correlation between serum uric acid(SUA)levels and incident chronic kidney disease(CKD)in middle-aged and elderly Chinese population and gender differences.Methods Based on the longitudinal survey data of China Health and Retirement Longitudinal Study from 2011 to 2015,the CKD-Epidemiology Collaboration cystatin C formula was used to estimate the glomerular filtration rate(eGFR),and 4 119 participants with normal renal function(eGFR≥60 mL·min-1·1.72 m-2)at baseline were included.Incident CKD was defined as eGFR<60 mL·min-1·1.72 m-2 at the follow-up in 2015.Logistic regression analysis was used to analysis the association of SUA levels at baseline and incident CKD among different genders.Restricted cubic spline analysis was used to analyze the dose-response relationship.Results After 4-year follow-up,127 participants developed incident CKD,including 57 males and 70 females.Multivariate Logistic regression analysis showed that elevated SUA levels were independently associated with the risk of incident CKD(OR=1.532,P<0.001).For each 1 mg/dL increase in SUA,the risk of incident CKD increased by 33.6%in males(OR=1.336,P=0.012)and 77.5%in females(OR=1.755,P<0.001).Restricted cubic spline analysis showed a linear positive correlation between SUA levels and incident CKD in both males and females.Participants were divided into four groups according to SUA quartiles(Q1-Q4).Multivariate Logistic regression analysis indicated a significant increase in the risk of incident CKD in Q3 group(3.75 mg/dL4.43 mg/dL)compared with Q1 group in females(Q3 group:OR=2.571,P=0.045;Q4 group:OR=3.666,P=0.005).Conclusion SUA is an independent risk factor for incident CKD in the middle-aged and elderly population.In females,serum uric acid levels exceeding 3.75 mg/dL are associated with an increased risk of incident CKD.

Objective To investigate the correlation between serum uric acid(SUA)levels and incident chronic kidney disease(CKD)in middle-aged and elderly Chinese population and gender differences.Methods Based on the longitudinal survey data of China Health and Retirement Longitudinal Study from 2011 to 2015,the CKD-Epidemiology Collaboration cystatin C formula was used to estimate the glomerular filtration rate(eGFR),and 4 119 participants with normal renal function(eGFR≥60 mL·min-1·1.72 m-2)at baseline were included.Incident CKD was defined as eGFR<60 mL·min-1·1.72 m-2 at the follow-up in 2015.Logistic regression analysis was used to analysis the association of SUA levels at baseline and incident CKD among different genders.Restricted cubic spline analysis was used to analyze the dose-response relationship.Results After 4-year follow-up,127 participants developed incident CKD,including 57 males and 70 females.Multivariate Logistic regression analysis showed that elevated SUA levels were independently associated with the risk of incident CKD(OR=1.532,P<0.001).For each 1 mg/dL increase in SUA,the risk of incident CKD increased by 33.6%in males(OR=1.336,P=0.012)and 77.5%in females(OR=1.755,P<0.001).Restricted cubic spline analysis showed a linear positive correlation between SUA levels and incident CKD in both males and females.Participants were divided into four groups according to SUA quartiles(Q1-Q4).Multivariate Logistic regression analysis indicated a significant increase in the risk of incident CKD in Q3 group(3.75 mg/dL4.43 mg/dL)compared with Q1 group in females(Q3 group:OR=2.571,P=0.045;Q4 group:OR=3.666,P=0.005).Conclusion SUA is an independent risk factor for incident CKD in the middle-aged and elderly population.In females,serum uric acid levels exceeding 3.75 mg/dL are associated with an increased risk of incident CKD.