This study evaluated the prognostic value of the C-PLAN index in advanced esophageal squamous cell carcinoma (ESCC) patients receiving immune checkpoint inhibitor (ICI) therapy. A retrospective analysis of 241 eligible patients treated during February 2020 to January 2023 was conducted. Based on the C-PLAN index, calculated from lactate dehydrogenase (LDH), C-reactive protein (CRP), performance status (PS), albumin (ALB), and derived neutrophil-to-lymphocyte ratio (dNLR), patients were categorized into Good (0-1 points) and Poor (2-5 points) groups. The Poor group exhibited more advanced clinical stages and larger tumor diameters (both p < 0.05). The Good group demonstrated a significantly higher objective response rate and disease control rate (both p < 0.05), lower progression/death incidence (both p < 0.001), and longer progression-free survival and overall survival (p < 0.001). Multifactorial Cox regression analysis revealed that PD-L1 CPS < 10%, clinical stage IV, and high C-PLAN score (2-5 points) were independent risk factors for disease progression or death following ICI therapy in patients with advanced ESCC. The C-PLAN index effectively stratifies prognosis and optimizes therapeutic decision-making for advanced ESCC. The C-PLAN index serves as a prognostic factor, providing an objective basis for survival assessment and treatment plan optimization in advanced ESCC patients.

Doxorubicin (DOX), a potent anthracycline chemotherapeutic, exhibits dose-dependent cardiotoxicity that limits its clinical utility. Although miR-145-5p demonstrates cardioprotective properties in cardiovascular diseases, its role in DOX-induced cardiomyopathy remains undefined. This study investigated the therapeutic potential of miR-145-5p against DOX-induced cardiotoxicity and its underlying mechanism. Wistar rats received cumulative DOX dosing (15 mg/kg total) to establish cardiotoxicity, with miR-145-5p overexpression achieved via adeno-associated virus serotype 9 (AAV9) delivery. Cardiac function was assessed by echocardiography and serum biomarkers, including creatine kinase-MB isoenzyme (CK-MB), cardiac troponin T (c-TnT), C-reactive protein (CRP), and N-terminal pro-B-type natriuretic peptide (NT-proBNP). Histopathology (Hematoxylin & Eosin/Masson's Trichrome staining), apoptosis (TUNEL), oxidative stress (dihydroethidium staining/malondialdehyde/glutathione), and NLRP3 inflammasome activation (ELISA/Western blot/immunohistochemistry) were evaluated. Clinical relevance was determined by quantifying serum miR-145-5p and SOX9 mRNA in healthy controls and breast cancer patients before and after DOX treatment. DOX significantly downregulated miR-145-5p and upregulated SOX9 in rat myocardium and H9C2 cells. DOX-treated patients displayed reduced serum miR-145-5p and increased SOX9 mRNA compared with pre-chemotherapy baselines. AAV9-miR-145-5p attenuated DOX-induced systolic dysfunction, reduced serum biomarkers, ameliorated histopathological injury and fibrosis, suppressed apoptosis and oxidative stress, and inhibited NLRP3 inflammasome activation (decreased NLRP3, ASC, caspase-1, IL-1β, and IL-18). miR-145-5p directly targeted the SOX9 3'UTR, and SOX9 overexpression reversed miR-145-5p-mediated reductions in CK release, ROS production, apoptosis, and NLRP3 expression in H9C2 cells. These findings demonstrate that miR-145-5p protects against DOX cardiotoxicity by targeting SOX9 to inhibit NLRP3 inflammasome-mediated pyroptosis, offering a potential therapeutic strategy.

Liver transplantation (LT) is the standard treatment for end-stage liver disease, yet the gap between the demand for organs and their availability is widening. In Taiwan, the scarcity of deceased donor organs highlights the need for optimized utilization strategies. The donor risk index (DRI) has emerged as a predictive tool for transplant outcomes, but existing models are not well-suited for Taiwan's unique demographic and clinical context. This retrospective cohort study analyzed a total of 118 deceased donor liver transplantation (DDLT) cases from Chang Gung Memorial Hospital between January 2020 and October 2023. Key demographic and clinical data were collected, focusing on one-year mortality and associated outcomes. Additionally, a retrospective validation cohort of 60 patients from January 2018 to December 2019 and a prospective validation cohort of 41 patients from November 2023 to August 2024 were included to assess the robustness of the CGMH-DRI model. Statistical analyses included univariate and multivariate logistic regression to identify independent risk factors. The study identified MELD 3.0 score, donor total bilirubin, and cold ischemia time (CIT) as independent predictors of one-year mortality. The CGMH-DRI model demonstrated good predictive performance (AUC = 0.778) for mortality, early allograft dysfunction (EAD), and major complications. Validation results showed consistent performance, with AUROC values of 0.716 in the retrospective cohort and 0.694 in the prospective cohort for one-year mortality; 0.781 and 0.676 for EAD; and 0.727 and 0.705 for major complications, respectively. The CGMH-DRI model offers a simple yet helpful tool for risk stratification in DDLT. It enables clinicians to identify high-risk patients and improve decision-making in liver transplantation. Further validation in diverse populations is warranted to enhance its applicability.

This study investigated the effects of histone lactylation on ferroptosis in hypoxia-induced cardiomyocytes. A hypoxia model was established in AC16 cells treated with 2-Deoxy-D-glucose (2-DG, a glucose analogue), ferrostatin-1 (Fer-1, a selective ferroptosis inhibitor), lactate (LA), sh-β-catenin (shRNA of β-catenin), or SKL2001 (an agonist of the Wnt/β-catenin pathway) for subsequent experiments. Hypoxia increased glycolysis ability, HK2, PDK1, and LDHA mRNA expression, HK and LDH activities, and LA levels in AC16 cells, decreased SLC7A11 and GPX4 protein levels and GSH levels, and elevated iron ion, MDA, and ROS levels, Wnt3 and nuclear β-catenin protein levels, β-catenin nucleus entry, the overall level of lactylation, the lactylation of β-catenin, and β-catenin protein stability. 2-DG or Fer-1 treatment reduced iron ion, MDA, and ROS levels but increased SLC7A11 and GPX4 protein levels and GSH levels in hypoxia-treated cells. 2-DG treatment decreased Wnt3 and nuclear β-catenin protein levels, β-catenin nucleus entry, the overall level of lactylation, the lactylation of β-catenin, and β-catenin protein stability, whereas LA treatment produced the opposite effects. Wnt/β-catenin pathway repression attenuated hypoxia-induced ferroptosis in cardiomyocytes. Collectively, hypoxia enhances histone lactylation, activates the Wnt/β-catenin pathway, and increases β-catenin stability, thereby promoting ferroptosis in cardiomyocytes.

Pediatric asthma is a common chronic airway inflammatory disease, where accurate assessment of disease severity and prognosis prediction is crucial for treatment decisions. Currently, there is a lack of precise and effective biomarkers. This study aimed to investigate the association between serum levels of lipocalin-2 (LCN2), soluble suppression of tumorigenicity 2 (sST2), and fibroblast growth factor 21 (FGF21) with asthma severity and to evaluate their predictive value for prognosis. A total of 110 asthmatic children (asthma group) were enrolled and stratified by severity into mild (n = 50), moderate (n = 34), and severe (n = 26) subgroups. After 4 weeks of treatment, the asthma group was further divided into good prognosis (n = 48) and poor prognosis (n = 64) subgroups based on Childhood Asthma Control Test (C-ACT) scores. Additionally, 110 healthy children were randomly selected as controls. Serum LCN2, sST2, and FGF21 levels were measured using enzyme-linked immunosorbent assay. Clinical data and pulmonary function parameters were collected. Spearman correlation analysis assessed the relationship between biomarker levels and C-ACT scores. Multivariate logistic regression identified risk factors for poor prognosis. Receiver operating characteristic (ROC) curve analysis evaluated the predictive performance of LCN2, sST2, and FGF21 for poor prognosis. Serum LCN2, sST2, and FGF21 levels were significantly higher in asthmatic children than in controls (p < 0.05), with levels progressively elevating as disease severity increased (p < 0.05). The good prognosis group exhibited lower levels of all three biomarkers compared to the poor prognosis group (p < 0.05). Spearman analysis revealed negative correlations between biomarker levels and C-ACT scores (p < 0.05). Multivariate logistic regression confirmed LCN2, sST2, and FGF21 as independent risk factors for poor prognosis (p < 0.05). ROC analysis demonstrated moderate predictive efficacy for individual biomarkers, while their combination achieved an area under the curve of 0.938, with 93.33% sensitivity and 90.00% specificity, suggesting potential clinical utility for severity assessment and prognosis prediction. Serum LCN2, sST2, and FGF21 levels increase with asthma severity and demonstrate high predictive value for poor prognosis when combined. These biomarkers may serve as early prognostic indicators in pediatric asthma management.

Osteoarthritis (OA) is a prevalent degenerative joint disease. This study combines bioinformatics analysis with in vivo and in vitro experiments to elucidate the molecular mechanisms through which melatonin (MT) regulates mitophagy to alleviate OA. Rat and chondrocyte OA models were established via anterior cruciate ligament transection or interleukin (IL)-1β induction, followed by treatment with MT, Cyclosporine A (a mitophagy inhibitor), and 740Y-P (a phosphatidylinositol-3 kinase [PI3K] activator). Pathological changes in cartilage, histological scores, and cell apoptosis were evaluated alongside chondrocyte viability, apoptosis, mitochondrial morphology, mitochondrial membrane potential, and mitophagy using H&E and Safranin O-fast green staining, Osteoarthritis Research Society International scoring (OARSI), TUNEL staining, CCK-8, flow cytometry, transmission electron microscopy, JC-1 staining, and immunofluorescence. Levels of inflammatory factors and mitophagy-related protein levels were determined by ELISA and western blot. Bioinformatics analysis was applied to investigate the regulatory mechanisms of MT on mitophagy in OA. In vivo, MT mitigated OA by enhancing mitophagy and reducing apoptosis of cartilage cells. In vitro, MT attenuated IL-1β-induced chondrocyte apoptosis through mitophagy activation, and this effect was partially reversed by mitophagy inhibition. Mechanistically, the PI3K/protein kinase B (AKT)/forkhead box O3 (FoxO3) axis appeared to play a central role. MT suppressed PI3K/AKT signaling, thereby upregulating FoxO3 expression and promoting mitophagy, ultimately reducing chondrocyte apoptosis. Collectively, these findings suggest that MT enhances mitophagy via inhibition of the PI3K/AKT pathway, and subsequent upregulation of FoxO3, leading to reduced apoptosis of cartilage cells and attenuation of OA progression in rats.

IgA nephropathy (IgAN), the most common form of glomerulonephritis, is a major and growing public health issue. It results from intestinal barrier dysfunction that leads to mesangial deposition of pathogenic galactose-deficient IgA1 (Gd-IgA1) and renal inflammation. This study aimed to investigate the therapeutic effects and associated mechanisms of forsythiaside A on intestinal barrier injury in IgAN in animal models. Rats were treated with bovine serum albumin (BSA), carbon tetrachloride (CCl), and lipopolysaccharide (LPS) to induce IgAN, followed by intragastric administration of forsythiaside A once daily from weeks 15 to 20 after model establishment. Biochemical markers, including 24-h urinary protein, blood urea nitrogen (BUN), serum creatinine (SCr), renal and intestinal tissue pathology, and levels of pro-inflammatory cytokines in the serum, kidney, and intestine, intestinal tight junction proteins, and TLR4/NF-κB pathway components were examined. The results showed that forsythiaside A decreased 24-h urinary protein, BUN, and SCr levels, alleviated renal damage, and attenuated glomerular and tubular lesions, collagen deposition, and glomerular IgA deposition in IgAN rats. Forsythiaside A treatment inhibited CD68-positive macrophage infiltration in renal tissues and downregulated serum and renal levels of IL-1β, IL-6, and TNF-α, while also alleviating intestinal barrier injury and intestinal inflammation, as shown by reduced levels of IL-1β, IL-6, and TNF-α and increased expression of the intestinal tight junction proteins occludin and ZO-1. Lastly, forsythiaside A treatment lowered serum LPS concentrations, as well as renal and intestinal levels of TLR4, p-NF-κB p65, and p-IκBα, and raised both renal and intestinal levels of IκBα. Collectively, forsythiaside A was found to ameliorate the progression of IgAN in rats by alleviating inflammation and intestinal barrier injury by suppression of TLR4/NF-κB signaling.

Glioblastoma (GBM) is an aggressive brain tumor with poor prognosis owing to its high invasiveness and resistance to therapy. RTA-408, a synthetic triterpenoid and nuclear factor erythroid 2-related factor 2 activator, exhibits anti-inflammatory and anti-cancer properties; however, its effects on GBM remain unclear. This study investigated the therapeutic potential of RTA-408 in GBM, focusing on its role in the activation of the JNK pathway. GBM8401 and A172 cells were treated with RTA-408, and cell viability, apoptosis, migration, and radiosensitivity were assessed. Western blot analysis was used to evaluate the epithelial-mesenchymal transition markers, cyclin D1, and JNK signaling. Intracranial xenograft models were used to assess tumor growth suppression by RTA-408 alone or in combination with radiotherapy. RTA-408 significantly reduced cell viability, induced apoptosis, and inhibited the migration of GBM cells, correlating with the activation of the JNK pathway. JNK inhibition reversed these effects, confirming its role in RTA-408-mediated tumor suppression. RTA-408 also enhanced radiosensitivity and reduced clonogenic survival. RTA-408 suppressed GBM tumor growth in vivo, with the greatest effect observed in combination with radiotherapy. RTA-408 exerts antitumour and radiosensitizing effects via activation of the JNK pathway and inhibits GBM progression. These findings highlight its potential as a novel therapeutic strategy for the treatment of GBM.

Acute coronary syndrome (ACS) is a clinical syndrome involving myocardial ischemia. This study aimed to elucidate the mechanism of TET3 in ACS-induced CMEC damage, thereby identifying a new target for ACS treatment. The expression of TET3 in ACS patients and healthy subjects was analyzed. CMECs were stimulated with ox-LDL and transfected with si-TET3 for the detection of TET3 RNA and protein levels. Cell proliferation, apoptosis, and angiogenesis were evaluated. Subsequently, m5C modification and TET3 enrichment on CCAT2 were assessed, and CCAT2 stability was measured. The binding relationships between CCAT2 and FUS and between FUS and TRIM14 mRNA were analyzed. Additionally, lncRNA CCAT2 inhibition or TRIM14 overexpression in combination with si-TET3 treatment was conducted to verify the underlying mechanism. TET3 was strongly expressed in serum from ACS patients and ox-LDL-stimulated CMECs, and silencing TET3 reduced ox-LDL-induced CMEC damage. TET3 removed m5C modification on CCAT2 to decrease CCAT2 stability and expression. With TRIM14, CCAT2 competes to bind to FUS to suppress TRIM14 expression. CCAT2 knockdown or TRIM14 overexpression partially reversed the protective effect of si-TET3 on CMEC damage. In conclusion, TET3 removed m5C modification to inhibit CCAT2 expression and reduced the binding relationship between CCAT2 and FUS to upregulate TRIM14, thereby exacerbating CMEC damage in ACS.

Spinal cord injury (SCI) is a severe trauma to the central nervous system that often leads to motor and sensory dysfunction in patients, severely affecting their quality of life. Autophagy plays a role in the pathological process of SCI, but the specific mechanism of autophagy in this case is unknown. COL1A1 and CD44, as potentially important genes in the autophagic process, may regulate the signaling pathway and thus affect the autophagic process through protein interactions. The aim of this study was to investigate the interaction between COL1A1 and CD44 and its mechanism of regulating autophagy through the JAK1/STAT3 pathway, providing new targets for SCI treatment. An SCI rat model was established, along with a PC12 cell model induced by oxygen-glucose deprivation (OGD). COL1A1 and CD44 in rat spinal cord tissues and cells were assessed using RT-qPCR and Western blot. Motor function in rats was assessed by BBB score, and the pathological conditions of the rat spinal cord tissues and neuronal numbers were observed by HE staining and Nissl staining. COL1A1 and CD44 localization in PC12 cells was confirmed via immunofluorescence analysis, and their targeting binding was verified by Co-IP. In the cell model, apoptosis, proliferation, and autophagy were evaluated through flow cytometry, CCK-8, and mRFP-GFP-LC3 transfection, respectively. The activation of the JAK1/STAT3 cascade in spinal cord tissues and PC12 cells was assessed, along with its function in the cell model. COL1A1 and CD44 were significantly overexpressed in spinal cord tissues of SCI rats and OGD-treated PC12 cells. COL1A1 silencing promoted functional recovery and autophagy after SCI in rats, ameliorated OGD-induced PC12 cell injury, upregulated autophagy proteins, and increased the number of autophagosomes and autolysosomes. COL1A1 was able to bind to CD44 in a targeting fashion and regulated the JAK1/STAT3 cascade. CD44 overexpression counteracted the positive effects of COL1A1 silencing on both the functional recovery of SCI rats and OGD-induced PC12 cell injury. COL1A1 targets and binds to CD44 to activate autophagy mediated by the JAK1/STAT3 signaling pathway, inhibiting functional recovery after SCI.

The long-term cumulative impact of metabolic syndrome (MS) on cognitive decline remains uncertain. This study investigated how changes in MS status over 10 years relate to cognition and whether sex modifies this relationship. A total of 766 participants (mean baseline age: 54 years) from the Kaohsiung Atherosclerosis Longitudinal Study were enrolled. MS was defined using the modified National Cholesterol Education Program Adult Treatment Panel III criteria for Asian populations. Participants were categorized into four groups based on changes in MS status over the 10-year follow-up: never MS, ever MS, new MS, and persistent MS. Cognition was assessed using the Chinese version of the Montreal Cognitive Assessment (MoCA). Multivariate regression models were adjusted for age, sex, education, smoking status, physical activity, alcohol consumption, anxiety and depression. The results showed that participants with persistent MS had lower MoCA scores (β = -0.08, adjusted p = 0.020) compared to those who never had MS, with impairments primarily in the memory and language domains. This adverse effect was observed only in women (β = -0.12, adjusted p = 0.004), while no significant association was found in men (β = -0.03, adjusted p = 0.628). Individuals with nonpersistent MS (either ever or new MS) did not show significant cognitive decline compared to those who never had MS. This study demonstrates that persistent MS over a decade is linked to cognitive decline, with a more pronounced effect in women. These findings highlight the importance of early MS intervention in midlife, particularly for women, to reduce the risk of cognitive deterioration later in life.

Hepatocellular carcinoma (HCC) is a heterogeneous malignancy characterized by high mortality rates. This article presents a discussion of the role of ZNF652 in HCC cell proliferation and apoptosis, thereby identifying a new target for HCC treatment. The expression levels of ZNF652, circRHOT1, and SLC38A6 in HCC and healthy cells were analyzed. Cell proliferation and apoptosis were subsequently validated. The binding relationships between ZNF652 and the circRHOT1 promoter and between circRHOT1 and KAT5 were validated. The recruitment of KAT5 and H3K27ac to the SLC38A6 promoter was assessed via ChIP. Combined experiments were carried out to verify the role of the circRHOT1/SLC38A6 pathway in HCC cell proliferation and apoptosis. ZNF652, circRHOT1, and SLC38A6 were upregulated in HCC cells. ZNF652 silencing inhibited HCC cell proliferation but promoted apoptosis. Mechanistically, ZNF652 increased circRHOT1 expression at the transcriptional level and recruited KAT5 to the SLC38A6 promoter to increase H3K27ac enrichment and activate SLC38A6 expression. Combined experiments revealed that overexpression of circRHOT1 or SLC38A6 could alleviate the effects of ZNF652 silencing on HCC cell proliferation and apoptosis. In conclusion, ZNF652 transcriptionally activated circRHOT1 expression, recruited KAT5 to the SLC38A6 promoter, increased H3K27ac enrichment, and activated SLC38A6 expression, thus promoting HCC cell proliferation and inhibiting apoptosis.

Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, with a 5-year survival rate of less than 20% and a high risk of recurrence despite advances in treatment. This study aimed to identify new therapeutic targets to increase the effectiveness of NSCLC treatments. We examined the role of USP54 in ferroptosis using an MTT assay and assessed the levels of reactive oxygen species (ROS), ferrous iron (Fe), and malondialdehyde (MDA). To explore the underlying molecular mechanism, the intermolecular interactions was assessed using coimmunoprecipitation (Co-IP), chromatin immunoprecipitation (ChIP), and dual-luciferase reporter assays. We found that USP54 expression was reduced in NSCLC and that its overexpression inhibited NSCLC cell proliferation while inducing ferroptosis, as indicated by increased ROS, Fe, and MDA levels, along with changes in SLC7A11, GPX4, and ACSL4 expression. Additionally, USP54 mediated the deubiquitination of FOXA2, decreasing its degradation. And FOXA2 promoted ACSL4 transcription, which further induced ferroptosis in NSCLC cells. In conclusion, USP54 promotes ferroptosis and inhibits NSCLC progression by stabilizing FOXA2, which in turn activates ACSL4 transcription. This study provides a theoretical foundation for the development of therapies targeting USP54 or ACSL4 for NSCLC treatment.

Sepsis is typified by organ failure due to an unchecked host reaction to infection. This study aims to explore the mechanism of ubiquitin-specific peptidase 7 (USP7) in sepsis with the involvement of intercellular adhesion molecule-1 (ICAM-1). A sepsis model was established using lipopolysaccharide (LPS) induction in WT and USP7 mice, and various assays were conducted to evaluate survival rates, organ damage, inflammatory markers, and protein interactions. The results revealed that USP7 expression increased in LPS-treated WT mice, and its interaction with ICAM-1 stabilized ICAM-1 through deubiquitination. USP7 knockout significantly elevated survival rates of septic mice. USP7 knockout reduced pulmonary inflammation, neutrophil extracellular trap (NET) formation, and myeloperoxidase and Cit-H3 levels in septic mice. Moreover, USP7 knockout lowered the levels of organ injury markers (creatine kinase-MB [CK-MB], troponin-I, and blood urea nitrogen [BUN]), liver enzymes (ALT and AST), and inflammatory markers (TNF-α, IL-1β, IL-6, and IL-8). Co-culture of bone marrow-derived macrophages (BMDMs) from WT mice with ICAM-1+ neutrophils elevated levels of TNF-α, IL-1β, and IL-6. These findings suggest that USP7 plays a critical role in driving sepsis-induced NET formation and inflammation by stabilizing ICAM-1. Targeting USP7 may represent a potential therapeutic approach to mitigate sepsis-related inflammation and organ damage.

This study investigated the mechanism of miR-127-3p in tumor cell stemness and docetaxel (DTX) resistance in triple-negative breast cancer (TNBC). hsa-miR-127-3p and KIF3B levels were predicted using databases and validated in TNBC and paracancerous tissues. KM survival curves were plotted to analyze the effect of miR-127-3p on patient survival. Pearson's analysis was used to determine the correlation between miR-127-3p and KIF3B mRNA in cancer tissues. Drug-resistant TNBC cell lines were established. After transfection, the cell viability, IC50, proliferation, migration, invasion, DTX resistance, apoptosis, and expression of the stemness markers SOX2, OCT4, and Nanog were detected. Databases were used to predict the downstream targets of miR-127-3p. The starBase database and dual-luciferase assay were used to predict and validate the binding relationship of miR-127-3p with KIF3B. Finally, the effect of miR-127-3p on transplanted tumors in TNBC nude mice was verified. miR-127-3p was expressed at low levels in TNBC tissues and was notably associated with shorter survival. Upregulation of miR-127-3p reduced TNBC cell stemness and DTX resistance. miR-127-3p targeted KIF3B. KIF3B overexpression averted the effect of miR-127-3p. miR-127-3p inhibited the growth of transplanted tumors in TNBC nude mice. Overall, miR-127-3p targets KIF3B, thereby reducing TNBC cell stemness and reversing DTX resistance.

The age-related decline in accommodative function after the age of 50 years corresponds with an increasing incidence of primary angle-closure disease (PACD); however, the interaction between this decline and PACD remains unexamined. Additionally, refractive error-accommodation associations in elderly individuals, which are critical for PACD pathophysiology, remain unclear, despite a prior pediatric focus. This study evaluated visual functions (including binocular vision, vergence function, and accommodation function) in patients diagnosed with PACD. A total of 51 patients (102 eyes) were included in this prospective study. The subjects were categorized into the following three groups: primary angle-closure/primary angle-closure glaucoma (PAC/PACG), primary angle-closure suspect (PACS), and a control group. Various parameters, including best-corrected near visual acuity, refractive error, Worth's 4 Dot test results, stereoacuity, vergence facility, accommodative facility (AF), and amplitude of accommodation (AMP), were measured and compared across the groups. A negative correlation was noted between AMP and refractive error (p < 0.001). After controlling for age and refractive error, no significant difference in AMP was detected; however, a statistically significant difference in AF was noted among the groups. PACS (p = 0.002) and PAC/PACG (p = 0.048) emerged as independent predictors of strong AF compared with normal controls. No significant differences in best-corrected near visual acuity, binocular vision, or vergence facility were observed between the groups. This research demonstrated that patients diagnosed with PACS and PAC/PACG exhibited stronger AF compared with the control group. Furthermore, a negative correlation between AMP and refractive error was observed within the elderly population. This research characterizes the correlation between refractive status and accommodative function, while establishing a link between accommodative function and PACD. Future studies on PACD pathogenesis and clinical management should prioritize accommodative function as a key research focus.