ObjectiveThis paper aims to investigate the protective effects of the Tanyu Tongzhi Youhua prescription（TYTZP） against myocardial ischemia/reperfusion injury in rats via regulation of the cyclic GMP-AMP synthase （cGAS）/stimulator of interferon genes （STING） signaling pathway. MethodsFifty-six 8-week-old male Sprague-Dawley （SD） rats were randomly divided into sham group， model group， ticagrelor group （32.4 mg·kg^-1）， RU320521 （RU.521cGAS inhibitors） group （5 mL·kg^-1）， groups of TYTZP with low dose （3.6 g·kg^-1）， medium dose （7.2 g·kg^-1）， and high dose （14.4 g·kg^-1）， with eight rats per group. The ticagrelor group and groups of TYTZP with different doses received pre-treatment for seven days according to their respective protocols. The RU.521 group received an intraperitoneal injection one hour before modeling. A rat model of the no-reflow phenomenon in myocardial ischemia/reperfusion injury was established by ligating the left anterior descending coronary artery in situ. Myocardial no-reflow area was determined by thioflavin staining. Histopathological morphology of myocardial tissue was observed via hematoxylin and eosin （HE） staining. Cardiac function was detected by echocardiography. Myocardial microcirculation function change was observed by using real-time myocardial contrast echocardiography. The myocardial enzyme levels in the serum were measured by serum biochemical analysis. The double-stranded DNA （dsDNA） levels were detected by using PicoGreen. The protein expression of cGAS， STING， and nuclear factor-κB （NF-κB） p65 in myocardial tissue was detected by Western blot. The levels of cardiac troponin Ⅰ （cTNⅠ）， cardiac troponin T （cTNT）， interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the peripheral blood were measured by enzyme-linked immunosorbent assay （ELISA）. ResultsCompared with the sham group， the model group showed a significantly increased myocardial no-reflow area （P<0.01）. Myocardial fiber rupture and disarray and inflammatory cell infiltration were observed by HE staining. The ultrasound results indicated that left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01） were significantly decreased. Real-time myocardial contrast echocardiography showed that the peak time of myocardial blood perfusion was significantly prolonged （P<0.01）， and the levels of creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， cTNⅠ， cTNT， and dsDNA were significantly elevated （P<0.01）. Western blot results showed that the myocardial protein expressions of cGAS， STING， and NF-κB p65 were upregulated （P<0.01）. ELISA results showed that the inflammatory factors in the serum such as IL-6， IL-1β， and TNF-α were increased （P<0.01）. Compared with the model group， the group of the TYTZP significantly reduced the levels of myocardial enzyme， troponins， and dsDNA （P<0.01， P<0.05）， improved cardiac function and myocardial microcirculation， alleviated histopathological morphology and inflammatory infiltration， inhibited activation of the cGAS/STING pathway， reduced the expression of NF-κB p65 （P<0.01， P<0.05）， and inhibited inflammatory response. ConclusionThe TYTZP mitigates the no-reflow phenomenon in myocardial ischemia/reperfusion injury， and its mechanism is associated with inhibiting the activation of the cGAS/STING pathway and attenuating inflammatory responses.

ObjectiveThis paper aims to investigate the protective effects of the Tanyu Tongzhi Youhua prescription（TYTZP） against myocardial ischemia/reperfusion injury in rats via regulation of the cyclic GMP-AMP synthase （cGAS）/stimulator of interferon genes （STING） signaling pathway. MethodsFifty-six 8-week-old male Sprague-Dawley （SD） rats were randomly divided into sham group， model group， ticagrelor group （32.4 mg·kg^-1）， RU320521 （RU.521cGAS inhibitors） group （5 mL·kg^-1）， groups of TYTZP with low dose （3.6 g·kg^-1）， medium dose （7.2 g·kg^-1）， and high dose （14.4 g·kg^-1）， with eight rats per group. The ticagrelor group and groups of TYTZP with different doses received pre-treatment for seven days according to their respective protocols. The RU.521 group received an intraperitoneal injection one hour before modeling. A rat model of the no-reflow phenomenon in myocardial ischemia/reperfusion injury was established by ligating the left anterior descending coronary artery in situ. Myocardial no-reflow area was determined by thioflavin staining. Histopathological morphology of myocardial tissue was observed via hematoxylin and eosin （HE） staining. Cardiac function was detected by echocardiography. Myocardial microcirculation function change was observed by using real-time myocardial contrast echocardiography. The myocardial enzyme levels in the serum were measured by serum biochemical analysis. The double-stranded DNA （dsDNA） levels were detected by using PicoGreen. The protein expression of cGAS， STING， and nuclear factor-κB （NF-κB） p65 in myocardial tissue was detected by Western blot. The levels of cardiac troponin Ⅰ （cTNⅠ）， cardiac troponin T （cTNT）， interleukin-6 （IL-6）， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the peripheral blood were measured by enzyme-linked immunosorbent assay （ELISA）. ResultsCompared with the sham group， the model group showed a significantly increased myocardial no-reflow area （P<0.01）. Myocardial fiber rupture and disarray and inflammatory cell infiltration were observed by HE staining. The ultrasound results indicated that left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） （P<0.01） were significantly decreased. Real-time myocardial contrast echocardiography showed that the peak time of myocardial blood perfusion was significantly prolonged （P<0.01）， and the levels of creatine kinase （CK）， creatine kinase isoenzyme （CK-MB）， lactate dehydrogenase （LDH）， cTNⅠ， cTNT， and dsDNA were significantly elevated （P<0.01）. Western blot results showed that the myocardial protein expressions of cGAS， STING， and NF-κB p65 were upregulated （P<0.01）. ELISA results showed that the inflammatory factors in the serum such as IL-6， IL-1β， and TNF-α were increased （P<0.01）. Compared with the model group， the group of the TYTZP significantly reduced the levels of myocardial enzyme， troponins， and dsDNA （P<0.01， P<0.05）， improved cardiac function and myocardial microcirculation， alleviated histopathological morphology and inflammatory infiltration， inhibited activation of the cGAS/STING pathway， reduced the expression of NF-κB p65 （P<0.01， P<0.05）， and inhibited inflammatory response. ConclusionThe TYTZP mitigates the no-reflow phenomenon in myocardial ischemia/reperfusion injury， and its mechanism is associated with inhibiting the activation of the cGAS/STING pathway and attenuating inflammatory responses.

Objective: To analyze the clinical characteristics and management strategies of metronidazole-associated Stevens-Johnson syndrome (SJS), and to provide a clinical basis for medication safety during the oral perioperative period. Methods: The study adhered to the tenets of the Declaration of Helsinki and was approved by the Ethics Committee of Stomatological Hospital of Xi'an Jiaotong University. A retrospective analysis was conducted on a case of SJS following mandibular impacted tooth extraction, for which the patient had taken metronidazole. Additionally, a literature review was performed by searching databases including China National Knowledge Infrastructure, Wanfang, PubMed, and Web of Science to identify reported cases of metronidazole-associated SJS. Demographic features, medication regimens, latency periods, clinical signs, interventions, and prognosis were analyzed. Results: The patient presented with lip swelling, extensive erosion and ulceration of the oral mucosa, and severe odynophagia. Scattered erythematous macules and bullae were observed on the trunk and extremities, with a positive Nikolsky sign. Additionally, there was erosion of the perineal skin and glans penis mucosa, along with skin desquamation of the scrotum. The patient with SJS was managed in the hospital by discontinuing metronidazole and administering sequential treatments, including glucocorticoids, immunomodulators, intravenous immunoglobulin, and plasma exchange. The condition gradually improved; after a 14-month follow-up, only mild dry eye remained, with no significant scarring of the skin or mucosa. However, delayed recognition of early warning signs resulted in delayed drug withdrawal and intervention. The literature review identified 6 additional cases (3 males, 3 females) with a median age of 45.5 years (range 31-61). Indications for metronidazole included postoperative sepsis prophylaxis after duodenal ulcer perforation repair, digestive system infections, mucosal diseases, pelvic inflammatory disease, septic cellulitis with pneumonia, and gingivitis. Administration routes comprised oral (n = 2), intravenous (n = 3), and topical (n = 1). The latency period from drug administration to onset ranged from 0.25 to 7 days (median 4 days). All of the cases presented with oral mucosal erosion, and a positive Nikolsky’s sign was noted for five patients. Discontinuation of the causative drug was the cornerstone of treatment, supplemented by immunomodulatory therapy, symptomatic support, and multidisciplinary collaboration. Prognoses varied significantly: among the four patients treated with “drug withdrawal + glucocorticoids + supportive care,” three recovered fully and one improved; among the two patients receiving “drug withdrawal + simple supportive care,” one recovered and one died Conclusion Although metronidazole-associated SJS is rare, it progresses rapidly and frequently involves oral mucosal damage, typically occurring within one week of administering the medication. Early drug withdrawal and prompt initiation of glucocorticoid therapy can improve prognosis. During the oral perioperative period, strict adherence to metronidazole indications, enhanced monitoring for early warning symptoms, and the establishment of a multidisciplinary collaborative diagnosis and treatment model are essential to minimize the risk of severe adverse drug reactions.

ObjectiveTo observe the effect of rehabilitation robot training on abdominal muscles thickness and balance ability in children with hemiplegia. MethodsFrom October, 2024 to December, 2025, 58 children with hemiplegia were admitted to Beijing Bo'ai Hospital and randomly divided into control group (n = 29) and experimental group (n = 29). Both groups received conventional rehabilitation treatment, and the experimental group received rehabilitation robot training in addition, for four weeks. The thickness of bilateral external oblique, internal oblique and transversus abdominis, Berg Balance Scale (BBS) score, the time of Timed Up and Go Test (TUGT), the center of pressure (COP) ellipse area, and self-selected walking speed (SWS) and maximum walking speed (MWS) of 10-meter walk test were compared before and after training. ResultsThree cases dropped out in each group. After training, the thickness of the external oblique, internal oblique and transverse abdominis on the hemiplegic side increased significantly in the experimental group (|t| > 7.280, P < 0.001, Cohen's d = 1.43~2.01), and was better in the experimental group than in the control group (|t| > 2.895, P < 0.01, Cohen's d = 0.80~1.60); the BBS score increased in both groups (|t| > 6.667, P < 0.001, Cohen's d = 1.30~4.06), and was better in the experimental group than in the control group (t = -2.721, P < 0.01, Cohen's d = 0.75). The time of TUGT decreased in both groups (t > 5.790, P < 0.001, Cohen's d = 1.14~2.68), and was better in the experimental group than in the control group (t = 2.290, P < 0.05, Cohen's d = 0.63). The SWS and MWS increased in both groups (|Z| > 2.910, P < 0.01, r = 0.40~0.68), and were better in the experimental group than in the control group (|Z| > 2.912, P < 0.05, r = 0.40~0.45), and the differences remained significant after correction. ConclusionRehabilitation robot training can improve the thickness of external oblique, the internal oblique and transversus abdominis muscles on the hemiplegic side in children with hemiplegia, and improve their balance and walking functions.

As a common type of primary liver cancer， hepatocellular carcinoma （HCC） is a major health threat in China. Ultrasound is a crucial imaging modality in the clinical diagnosis and treatment of HCC， and the development and application of new ultrasound technologies have high clinical value. Currently， ultrasound and contrast-enhanced ultrasound combined with artificial intelligence have shown promising potential in the detection of focal liver lesions， image-based HCC diagnosis， outcome assessment， and prognostic prediction； furthermore， ultrasound fusion imaging technology has shown certain clinical value in guidance and efficacy evaluation of percutaneous thermal ablation； three-dimensional ultrasound has certain advantages in assisting ablation and assessing ablation margins； endoscopic ultrasonography can be used as a supplementary method for HCC cases that are difficult to scan or guide via percutaneous ultrasound.

ObjectiveTo investigate the impact of Buzhong Yiqitang combined with cisplatin on the proliferation of human lung adenocarcinoma （A549） cells through regulation of the pyruvate dehydrogenase kinase 1 （PDK1）/protein kinase B （Akt） signaling pathway and influence on glycolysis. MethodsTranscriptome sequencing （RNA-seq） was employed to compare the expression of glycolysis-related genes between A549 cells and cisplatin-resistant human lung adenocarcinoma cells （A549/DDP）. Small interfering RNA （siRNA） was employed to knock down PDK1， and the knockdown efficiency was verified by Western blot and Read-time PCR. The cell counting kit-8 （CCK-8） assay was used to assess the survival and viability of A549 cells under the following conditions： siRNA negative control+cisplatin （128， 64， 32， 16， 8， 4， 0 μmol·L^-1）， siPDK1+cisplatin （128， 64， 32， 16， 8， 4， 0 μmol·L^-1）， and siPDK1+cisplatin （128， 64， 32， 16， 8， 4， 0 μmol·L^-1）+Buzhong Yiqitang （10%）-containing serum. The 20% inhibitory concentration （IC₂₀） of the siRNA negative control+cisplatin group （7.832 μmol·L^-1） was calculated and used as the subsequent cisplatin concentration. Colony formation assay was performed to evaluate the proliferation of A549 cells. Lactate and adenosine triphosphate （ATP） assay kits were used to measure lactate and ATP production. The mitochondrial membrane potential was detected with the fluorescent probe JC-1. Western blotting was conducted to examine the expression levels of PDK1， phosphorylated （p）-Akt， Akt， pyruvate kinase M2 （PKM2）， glucose transporter 1 （GLUT1）， pyruvate dehydrogenase （PDH）， and lactate dehydrogenase A （LDHA）. Confocal immunofluorescence was employed to detect PDK1 and p-Akt. ResultsRNA-seq results identified PDK1 as a highly expressed differential gene in glycolysis metabolism between A549 cells and A549/DDP cells， and it was highly expressed in tumor cells. Gene Set Enrichment Analysis （GSEA） revealed upregulated and downregulated genes in glycolysis and gluconeogenesis pathways. Western blot and RT-qPCR confirmed that PDK1-si-2 had the highest transfection efficiency， with a PDK1 knockdown rate exceeding 60%. CCK-8 assay determined the half-maximal inhibitory concentration （IC₅₀） values for each group as （30.698±5.348）， （16.372±3.562）， （13.237±1.573） μmol·L^-1， while the IC₂₀ of cisplatin in siRNA negative control-transfected A549 cells was （7.832±0.672） μmol·L^-1. Compared with the siRNA negative control group， the siRNA negative control+cisplatin group showed decreased colony formation rate， reduced lactate production， lowered mitochondrial membrane potential， downregulated protein levels of p-Akt， GLUT1， PDK1， PDH， and LDHA， and reduced PDK1 fluorescence intensity （P<0.05）. The siPDK1 group exhibited decreased colony formation rate， reduced lactate production， increased ATP production， lowered mitochondrial membrane potential， downregulated protein levels of p-Akt， PKM2， GLUT1， PDK1， PDH， and LDHA， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. Compared with the siPDK1 group， the siPDK1+Buzhong Yiqitang group showed decreased colony formation rate， reduced lactate production， downregulated protein levels of PKM2， GLUT1， and PDK1， and reduced PDK1 fluorescence intensity （P<0.05）. The siPDK1+cisplatin group exhibited decreased colony formation rate， reduced lactate production， increased ATP production， lowered mitochondrial membrane potential， downregulated protein levels of PKM2， GLUT1， PDK1， and PDH， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. The siPDK1+cisplatin+Buzhong Yiqitang group demonstrated decreased colony formation rate， reduced lactate production， increased ATP production， lowered mitochondrial membrane potential， downregulated protein levels of p-Akt， PKM2， GLUT1， PDK1， PDH， and LDHA， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. Compared with the siPDK1+Buzhong Yiqitang group， the siPDK1+cisplatin group showed decreased colony formation rate， downregulated protein levels of p-Akt and PDH， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. The siPDK1+cisplatin+Buzhong Yiqitang group exhibited decreased colony formation rate， reduced lactate production， increased ATP production， lowered mitochondrial membrane potential， downregulated protein levels of p-Akt， GLUT1， PDH， and LDHA， and reduced PDK1 and p-Akt fluorescence intensity （P<0.05）. Compared with the siPDK1+cisplatin group， the siPDK1+cisplatin+Buzhong Yiqitang group showed decreased colony formation rate， increased ATP production， and downregulated protein levels of p-Akt， PKM2， and LDHA （P<0.05）. ConclusionBuzhong Yiqitang combined with cisplatin can suppress lung adenocarcinoma cell proliferation by modulating glycolysis through the PDK1/Akt signaling pathway.

ObjectiveTo clarify the anti-inflammatory and lung-protective effects of Yantiao prescription on lipopolysaccharide （LPS）-induced acute lung injury （ALI）， and to explore the impact of Yantiao prescription on the metabolic pathways of arachidonic acid （AA） in vivo. MethodsThirty male C57BL/6J mice were randomly divided into the following groups based on body weight： normal group， model group， dexamethasone group （2 mg·kg^-1）， low-dose Yantiao prescription group （18 g·kg^-1）， and high-dose Yantiao prescription group （36 g·kg^-1）， with 6 mice in each group. The ALI mouse model was established by intraperitoneal injection of LPS. The treatment groups received oral gavage once a day for 7 consecutive days， and serum and lung tissue were collected at the end of the experiment. The content of pro-inflammatory cytokines tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） in serum was detected by enzyme-linked immunosorbent assay （ELISA）. Hematoxylin-eosin （HE） staining was used to assess lung tissue pathology. The wet/dry weight ratio （W/D） and myeloperoxidase （MPO） activity in lung tissue were measured. The content of AA metabolites in serum and lung tissue was measured by liquid chromatography triple quadrupole-mass spectrometry （LC-MS/MS）. ResultsCompared with the conditions in the normal group， the content of serum pro-inflammatory cytokines TNF-α， IL-1β， and IL-6 in the model group was significantly increased （P<0.01）. The alveolar structure in mice was severely damaged， with markedly thickened alveolar walls and extensive inflammatory cell infiltration. The W/D ratio and MPO activity in lung tissue were significantly increased （P<0.01）. The content of AA metabolites， including prostaglandin D₂ （PGD₂）， prostaglandin E₂ （PGE₂）， 11（S）-hydroxy-eicosatetraenoic acid ［11（S）-HETE］， and 5-hydroxy-eicosatetraenoic acid （5-HETE） in serum and lung tissue was significantly increased （P<0.05）， while the content of 11，12-epoxyeicosatrienoic acid （11，12-EET） and 14，15-epoxyeicosatrienoic acid （14，15-EET） in serum was significantly decreased （P<0.01）. Compared with the results in the model group， the content of serum pro-inflammatory cytokines TNF-α， IL-1β， and IL-6 in the dexamethasone group， low-dose Yantiao prescription group， and high-dose Yantiao prescription group was significantly reduced （P<0.05）. Mild thickening of alveolar walls， scattered inflammatory cell infiltration， and relatively intact tissue structure with improved alveolar architecture were observed. The W/D ratio and MPO activity in lung tissue were significantly reduced （P<0.01）. The content of AA metabolites PGD₂， PGE₂， 11（S）-HETE， and 5-HETE in serum from the dexamethasone group was significantly decreased （P<0.05）， while the content of 14，15-EET in serum significantly increased （P<0.01）， and the content of 5-HETE in lung tissue significantly decreased （P<0.01）. In the low-dose and high-dose Yantiao prescription groups， the content of AA metabolites PGD₂， PGE₂， 11（S）-HETE， and 5-HETE in serum and lung tissue was significantly decreased （P<0.05）， while the content of 11，12-EET in both serum and lung tissue was significantly increased （P<0.05）. ConclusionYantiao prescription has significant protective effects against LPS-induced ALI， which are related to its regulation of AA metabolic pathways in vivo.

Objective This study aimed to analyze the characteristics and clinical significance of peripheral lymphocytic subsets and cytokine levels, including interleukin 1β(IL-1β), IL-2, IL-4, IL-5, IL-6, IL-8, IL-10, IL-12P70, IL-17A, tumor necrosis factor α(TNF-α), interferon γ(IFN-γ) and IFN-α, in patients with primary biliary cholangitis (PBC), to provide some novel insights into the pathogenesis of PBC. Methods We retrospectively collected clinical features and laboratory data from hospitalized patients who were primarily diagnosed with PBC and from healthy physical examinees at the Third People's Hospital of Changzhou between January 1, 2023, and June 30, 2024. Results A total of 152 PBC patients and 96 healthy controls who met the inclusion and exclusion criteria were enrolled. Significant differences were observed in baseline characteristics and laboratory data between the two groups. After the propensity score matching (PSM) analysis, 61 PBC patients and 61 healthy controls were successfully matched, ensuring that the general characteristics (age and gender) of the two groups were balanced and comparable. Compared to the control group, the proportion of peripheral lymphocytes was significantly higher in the PBC group (31.9% vs. 17.8%), primarily due to an increase in CD4⁺ T cells (46.77% vs. 41.19%), while CD8⁺T cells were significantly decreased (19.73% vs. 22.07%). Notably, the proportions of CD4⁺ programmed cell death 1 (PD-1)⁺ T and CD8⁺PD-1⁺ T cells were elevated, with CD8⁺PD-1⁺ T cells showing a significant positive correlation with the severity of liver inflammation (r=0.41). Furthermore, the mitochondrial mass (MM) of CD4⁺ T cells was significantly increased in PBC patients, whereas no significant changes were observed in the MM of CD8⁺ T cells or the mitochondrial membrane potential (MMP) of CD3⁺ T cells. Additionally, the plasma levels of cytokines, such as IL-4, IL-8, IL-10 and IFN-α, were abnormally elevated. The plasma levels of IL-5 and IL-1β were negatively correlated with the stage of liver fibrosis in patients with PBC (r=-0.52). Conclusion The overactivation and proliferation of CD4⁺ T cells, along with the suppression of CD8⁺ T cell function and increased PD-1 expression leads to T cell exhaustion, indicating significant immunological alterations in PBC patients. These changes are closely associated with the disease progression. Additionally, cytokines are likely involved in the immune regulation process of PBC and may influence the pathogenic mechanisms of the disease. Regular monitoring of lymphocyte subsets and cytokine levels can help assess the immune status and disease activity in patients with PBC, thereby guiding the individualized treatment strategies.
Humans ; Male ; Female ; Middle Aged ; Liver Cirrhosis, Biliary/blood* ; Retrospective Studies ; T-Lymphocyte Subsets/immunology* ; Aged ; Cytokines/blood* ; Adult ; CD8-Positive T-Lymphocytes/immunology*

Antibody-drug conjugates (ADCs) are antitumor drugs composed of monoclonal antibodies and cytotoxic payload covalently coupled by a linker. Currently, 15 ADCs have been clinically approved worldwide. More than 100 clinical trials at different phases are underway to investigate the newly developed ADCs. ADCs represent one of the fastest growing classes of targeted antitumor drugs in oncology drug development. It takes advantage of the specific targeting of tumor-specific antigen by antibodies to deliver cytotoxic chemotherapeutic drugs precisely to tumor cells, thereby producing promising antitumor efficacy and favorable adverse effect profiles. However, emergence of drug resistance has severely hindered the clinical efficacy of ADCs. In this review, we introduce the structure and mechanism of ADCs, describe the development of ADCs, summarized the latest research about the mechanisms of ADC resistance, discussed the strategies to overcome ADCs resistance, and predicted biomarkers for treatment response to ADC, aiming to contribute to the development of ADCs in the future.

This study investigated the role of the nuclear factor of activated T cells c3 (NFATc3) in vascular smooth muscle cells (VSMCs) during aortic aneurysm and dissection (AAD) progression and the underlying molecular mechanisms. Cytoplasmic and nuclear NFATc3 levels were elevated in human and mouse AAD. VSMC-NFATc3 deletion reduced thoracic AAD (TAAD) and abdominal aortic aneurysm (AAA) progression in mice, contrary to VSMC-NFATc3 overexpression. VSMC-NFATc3 deletion reduced extracellular matrix (ECM) degradation and maintained the VSMC contractile phenotype. Nuclear NFATc3 targeted and transcriptionally upregulated matrix metalloproteinase 9 (MMP9) and MMP2, promoting ECM degradation and AAD development. NFATc3 promoted VSMC phenotypic switching by binding to eukaryotic elongation factor 2 (eEF2) and inhibiting its phosphorylation in the VSMC cytoplasm. Restoring eEF2 reversed the beneficial effects in VSMC-specific NFATc3-knockout mice. Cabamiquine-targets eEF2 and inhibits protein synthesis-inhibited AAD development and progression in VSMC-NFATc3-overexpressing mice. VSMC-NFATc3 promoted VSMC switch and ECM degradation while exacerbating AAD development, making it a novel potential therapeutic target for preventing and treating AAD.