Case Report: A rare transthyretin mutation p.D58Y in a Chinese case of transthyretin amyloid cardiomyopathy.

Hereditary transthyretin amyloid (ATTRv) cardiomyopathy (CM) is caused by mutations in the TTR gene. TTR mutations contribute to TTR tetramer destabilization and dissociation, leading to excessive deposition of insoluble amyloid fibrils in the myocardium and finally resulting in cardiac dysfunction. In this article, we report a case of a Chinese patient with transthyretin mutation p.D58Y and provide detailed information on cardiac amyloidosis, including transthoracic echocardiography, cardiac magnetic resonance, and SPECT imaging for the first time. Our report aims to provide a better understanding of ATTR genotypes and phenotypes.

The value of urinary exosomal microRNA-21 in the early diagnosis and prognosis of bladder cancer.

Bladder cancer (BC) poses high morbidity and mortality, with urinary exosomal microRNA (miR)-21 showing potential value in its diagnosis and prognosis, and we probed its specific role. We prospectively selected 116 BC patients and 116 healthy volunteers as the BC and control groups, respectively. BC urinary exosomal miR-146a-5p, miR-93-5p, miR-663b, miR-21, and miR-4454 relative expression levels were assessed. The correlations between clinical indexes and urinary exosomal miR-21, prognostic value of miR-21, and diagnostic value of the five candidate miRNAs, urine cytology, and miRNA joint diagnostic panel for BC and urinary exosomal miR-21, miR-4454, and urine cytology for Ta-T1 and T2-T4 stage BC were analyzed. Urinary exosomal miR-146a-5p, miR-93-5p, miR-663b, miR-21, and miR-4454 were highly expressed in BC patients. miR-146a-5p, miR-93-5p, miR-663b, miR-21, miR-4454, miRNA combined diagnostic panel, and urine cytology had certain diagnostic value for BC, with miR-21, miR-4454, and miRNA co-diagnostic panel showing the highest diagnostic value. Collectively, urinary exosomal miR-21 was closely related to Tumor-Node-Metastasis staging and grading in BC patients. Urinary exosomal miR-21 had high diagnostic value for BC and Ta-T1 and T2-T4 stage BC, and had high predictive value for BC poor prognosis, providing an effective indicator for the occurrence, development, and prognostic assessment of BC.

Effect of the extrahepatic bile duct anatomy on choledocholithiasis and its clinical significance.

BACKGROUND: A comprehensive understanding of the extrahepatic bile duct anatomy is vital to guide surgical procedures and perform endoscopic retrograde cholangiography. Anatomical irregularities within the extrahepatic bile duct may increase susceptibility to bile duct stones. AIM: To investigate the anatomical risk factors associated with extrahepatic bile ducts in patients diagnosed with choledocholithiasis, with a specific focus on preventing stone recurrence after surgical intervention and endoscopic lithotomy. METHODS: We retrospectively analyzed the medical records of 124 patients without choledocholithiasis and 108 with confirmed choledocholithiasis who underwent magnetic resonance cholangiopancreatography examinations at our center between January 2022 and October 2022. Logistic regression analyses were conducted to identify the anatomical risk factors influencing the incidence of common bile duct stones. RESULTS: Multivariate logistic regression analysis revealed that several factors independently contributed to choledocholithiasis risk. Significant independent risk factors for choledocholithiasis were diameter of the common hepatic [adjusted odds ratio (aOR) = 1.43, 95% confidence interval (CI): 1.07-1.92, adjusted P value = 0.016] and common bile (aOR = 1.68, 95%CI: 1.27-2.23, adjusted P value < 0.001) ducts, length of the common hepatic duct (aOR = 0.92, 95%CI: 0.84-0.99, adjusted P value = 0.034), and angle of the common bile duct (aOR = 0.92, 95%CI: 0.89-0.95, adjusted P value < 0.001). CONCLUSION: The anatomical features of the extrahepatic bile duct were directly associated with choledocholithiasis risk. Key risk factors include an enlarged diameter of the common hepatic and bile ducts, a shorter length of the common hepatic duct, and a reduced angle of the common bile duct.

Innovative Formulation Platform: Paving the Way for Superior Protein Therapeutics with Enhanced Efficacy and Broadened Applications.

Protein therapeutics offer high therapeutic potency and specificity, the broader adoptions and development of protein therapeutics, however, have been constricted by their intrinsic limitations such as inadequate stability, immunogenicity, suboptimal pharmacokinetics and biodistribution, and off-target effects. This review describes a platform technology that formulates individual protein molecules with a thin formulation layer of crosslinked polymers, which confers the protein therapeutics with high activity, enhanced stability, controlled release capability, reduced immunogenicity, improved pharmacokinetics and biodistribution, and ability to cross the blood brain barriers. Based on currently approved protein therapeutics, this formulating platform affords the development of a vast family of superior protein therapeutics with improved efficacy and broadened indications at significantly reduced cost. This article is protected by copyright. All rights reserved.

Analysis of the factors influencing of sleep quality in intensive care unit awake patients based on a structural equation model: A cross-sectional study.

OBJECTIVE: The objective of this study was to construct and validate a structural equation model (SEM) to identify factors associated with sleep quality in awake patients in the intensive care unit (ICU) and to assist in the development of clinical intervention strategies. RESEARCH METHODS/SETTING: In this cross-sectional study, 200 awake patients who were cared for in the ICU of a tertiary hospital in China were surveyed via several self-report questionnaires and wearable actigraphy sleep monitoring devices. Based on the collected data, structural equation modelling analysis was performed using SPSS and AMOS statistical analysis software. The study is reported using the STROBE checklist. RESULTS: The fit indices of the SEM were acceptable: χ2/df = 1.676 (p < .001) and RMSEA = .058 (p < 0.080). Anxiety/depression had a direct negative effect on the sleep quality of awake patients cared for in the ICU (ß = -.440, p < .001). In addition, disease-freeness progress had an indirect negative effect on the sleep quality of awake patients cared for in the ICU (ß = -.142, p < .001). Analgesics had an indirect negative effect on the sleep quality of awake patients cared for in the ICU through pain and sedatives (ß = -.082, p < .001). Sedation had a direct positive effect on the sleep quality of conscious patients cared for in the ICU (ß = .493; p < .001). CONCLUSION: The results of the SEM showed that the sleep quality of awake patients cared for in the ICU is mainly affected by psychological and disease-related factors, especially anxiety, depression and pain, so we can improve the sleep quality of patients through psychological intervention and drug intervention.

Deoxynivalenol Induces Intestinal Epithelial Barrier Damage through RhoA/ROCK Pathway-Mediated Apoptosis and F-Actin-Associated Tight Junction Disruption.

Deoxynivalenol (DON) poses a serious global food safety risk due to its high toxicity and contamination rate. It disrupts the intestinal epithelial barrier, allowing exogenous toxins to enter the circulation and resulting in sepsis and systemic toxicity. In this research, 32 male Kunming mice and Porcine Small Intestinal Epithelial (IPEC-J2) cells were treated with DON at 0-4.8 mg/kg (7 d) and 0-12 µM (24 h), respectively. Histopathological results revealed that DON disrupted the intestinal epithelial barrier, causing apoptosis and tight junction (TJ) injury. Immunofluorescence and protein expression results showed that DON-induced p53-dependent mitochondrial pathway apoptosis and fibrillar actin (F-actin)-associated TJ injury and that the RhoA/ROCK pathway were activated in mice jejunal tissue and IPEC-J2 cells. Pretreatment with RhoA or ROCK inhibitors (Rosin or Y-27632) maintained DON-induced apoptosis and F-actin-associated TJ injury in IPEC-J2 cells. Thus, DON induces damage to the intestinal epithelial barrier through the RhoA/ROCK pathway-mediated apoptosis and F-actin-associated TJ disruption.

Genetically identified mediators associated with increased risk of stroke and cardiovascular disease in individuals with autism spectrum disorder.

Growing evidence suggested that individuals with autism spectrum disorder (ASD) associated with stroke and cardiovascular disease (CVD). However, the causal association between ASD and the risk of stroke and CVD remains unclear. To validate this, we performed two-sample Mendelian randomization (MR) and two-step mediation MR analyses, using relevant genetic variants sourced from the largest genome-wide association studies (GWASs). Two-sample MR evidence indicated causal relationships between ASD and any stroke (OR = 1.1184, 95% CI: 1.0302-1.2142, P < 0.01), ischemic stroke (IS) (OR = 1.1157, 95% CI: 1.0237-1.2160, P = 0.01), large-artery atherosclerotic stroke (LAS) (OR = 1.2902, 95% CI: 1.0395-1.6013, P = 0.02), atrial fibrillation (AF) (OR = 1.0820, 95% CI: 1.0019-1.1684, P = 0.04), and heart failure (HF) (OR = 1.1018, 95% CI: 1.0007-1.2132, P = 0.05). Additionally, two-step mediation MR suggested that type 2 diabetes mellitus (T2DM) partially mediated this effect (OR = 1.14, 95%CI: 1.02-1.28, P = 0.03). The mediated proportion were 10.96% (95% CI: 0.58%-12.10%) for any stroke, 11.77% (95% CI: 10.58%-12.97%) for IS, 10.62% (95% CI: 8.04%-13.20%) for LAS, and 7.57% (95% CI: 6.79%-8.36%) for HF. However, no mediated effect was observed between ASD and AF risk. These findings have implications for the development of prevention strategies and interventions for stroke and CVD in patients with ASD.

Squalene Epoxidase: Its Regulations and Links with Cancers.

Squalene epoxidase (SQLE) is a key enzyme in the mevalonate-cholesterol pathway that plays a critical role in cellular physiological processes. It converts squalene to 2,3-epoxysqualene and catalyzes the first oxygenation step in the pathway. Recently, intensive efforts have been made to extend the current knowledge of SQLE in cancers through functional and mechanistic studies. However, the underlying mechanisms and the role of SQLE in cancers have not been fully elucidated yet. In this review, we retrospected current knowledge of SQLE as a rate-limiting enzyme in the mevalonate-cholesterol pathway, while shedding light on its potential as a diagnostic and prognostic marker, and revealed its therapeutic values in cancers. We showed that SQLE is regulated at different levels and is involved in the crosstalk with iron-dependent cell death. Particularly, we systemically reviewed the research findings on the role of SQLE in different cancers. Finally, we discussed the therapeutic implications of SQLE inhibitors and summarized their potential clinical values. Overall, this review discussed the multifaceted mechanisms that involve SQLE to present a vivid panorama of SQLE in cancers.

Effects of stand-alone polar residue on membrane protein stability and structure.

Helical membrane proteins generally have a hydrophobic nature, with apolar side chains comprising the majority of the transmembrane (TM) helices. However, whenever polar side chains are present in the TM domain, they often exert a crucial role in structural interactions with other polar residues, such as TM helix associations and oligomerization. Moreover, polar residues in the TM region also often participate in protein functions, such as the Schiff base bonding between Lys residues and retinal in rhodopsin-like membrane proteins. Although many studies have focused on these functional polar residues, our understanding of stand-alone polar residues that are energetically unfavored in TM helixes is limited. Here, we adopted bacteriorhodopsin (bR) as a model system and systematically mutated 17 of its apolar Leu or Phe residues to polar Asn. Stability measurements of the resulting mutants revealed that all of these polar substitutions reduced bR stability to various extents, and the extent of destabilization of each mutant bR is also correlated to different structural factors, such as the relative accessible surface area and membrane depth of the mutation site. Structural analyses of these Asn residues revealed that they form sidechain-to-backbone hydrogen bonds that alleviate the unfavorable energetics in hydrophobic and apolar surroundings. Our results indicate that membrane proteins are able to accommodate certain stand-alone polar residues in the TM region without disrupting overall structures.

Iterative Pulse-Echo Tomography for Ultrasonic Image Correction.

Acoustic aberration, caused by the uneven distribution of tissue speed-of-sound (SoS), significantly reduces the quality of ultrasound imaging. An important approach to mitigate this issue is imaging correction based on local SoS estimation. Computed ultrasound tomography in echo mode (CUTE) is an SoS estimation method that utilizes phase-shift information from ultrasound pulse-echo signals, offering both practical utility and computational efficiency. However, the traditional single-pass CUTE often suffers from poor accuracy and robustness. In this paper, an advanced approach known as iterative CUTE is introduced, which refines SoS estimates through iterative correction of errors and noise, addressing the limitations of traditional single-pass methods. It is argued that traditional precision indicators like root mean square error (RMSE) fall short in adequately reflecting the quality of SoS estimates for imaging correction, and coherence factor (CF) is proposed as a more indicative metric. Performance validation of the iterative CUTE algorithm was conducted using a simulation and agar phantom experiment. The results indicated that the iterative CUTE approach surpasses the single-pass approach, enhancing the average CF for SoS estimates by up to 18.2%. In phantom experiments, imaging corrected with SoS estimates from iterative CUTE reduced the Array Performance Index (API) by up to 40% compared to traditional methods.

Structural Characterization and In Vitro Antioxidant Activity of a Novel Polysaccharide from Summer-Autumn Tea.

To enhance the utilization of summer-autumn tea, a water-soluble polysaccharide (D1N1) was isolated through a series of techniques including hot water extraction, ethanol precipitation, and column chromatography. The structure of D1N1 was determined through the utilization of ultraviolet, Fourier-transform infrared, high-performance anion-exchange chromatography, gas chromatography-tandem mass spectrometry, and nuclear magnetic resonance. The results revealed that glucose was the predominant component of D1N1, accounting for 95% of its composition. Additionally, D1N1 also contained galactose, arabinose, and rhamnose. The molecular weight (Mw) of D1N1 was determined to be 224.71 kDa. The backbone of D1N1 consisted of →4)-α-D -Glcp (1→, →3,4)-α-D-Galp-(1→, →4,6)-α-D -Glcp (1→ at a molar ratio of 35:1:1, and branching at the O-3 position of →3,4)-α-D-Galp-(1→ and O-6 position of →4,6)-α-D-Glcp (1→ with α-D -Glcp (1→. In addition, the antioxidant activity of D1N1 was also evaluated. D1N1 exhibited excellent antioxidant bioactivity against the DPPH, superoxide anion radical, and ABTS+ radical. These findings provide a theoretical basis for the application of summer-autumn tea polysaccharide as a potential functional food.

Viscoelastic polyacrylamide MR elastography phantoms with tunable damping ratio independent of shear stiffness.

Physiologically modeled test samples with known properties and characteristics, or phantoms, are essential for developing sensitive, repeatable, and accurate quantitative MRI techniques. Magnetic resonance elastography (MRE) is one such technique used to estimate tissue mechanical properties, and it is advantageous to use phantoms with independently tunable mechanical properties to benchmark the accuracy of MRE methods. Phantoms with tunable shear stiffness are commonly used for MRE, but tuning the viscosity or damping ratio has proven to be difficult. A promising candidate for MRE phantoms with tunable damping ratio is polyacrylamide (PAA). While pure PAA has very low attenuation, viscoelastic hydrogels have been made by entrapping linear polyacrylamide strands (LPAA) within the PAA network. In this study, we evaluate the use of LPAA/PAA gels as physiologically accurate phantoms with tunable damping ratio, independent of shear stiffness, via MRE. Phantoms were made with 15.3 wt% PAA while the LPAA concentration ranged from 4.5 wt% to 8.0 wt%. MRE was performed at 9.4 T with 400 Hz vibration on all phantoms revealing a strong, positive correlation between damping ratio and LPAA content (p < 0.001). There was no significant correlation between shear stiffness and LPAA content, confirming a constant PAA concentration yielded constant shear stiffness. Rheometry at 10 Hz was performed to verify the damping ratio of the phantoms. Nearly identical slopes for damping ratio versus LPAA content were found from both MRE and rheometry (0.0073 and 0.0075 respectively). Ultimately, this study validates the adaptation of polyacrylamide gels into physiologically-relevant MRE phantoms to enable testing of MRE estimates of damping ratio.

Facile fabrication of microfibrillated cellulose-based aerogels incorporated with nisin/ß-cyclodextrin microcapsule for channel catfish preservation.

In this study, a hydrophobic and antibacterial pad was prepared to preserve Channel Catfish (Ictalurus punctatus). The pad composite the microfibrillated cellulose and ß-cyclodextrin/nisin microcapsules. The hydrophobic pad ensures a dry surface in contact with the fish, reducing microbial contamination. The pad has a low density and high porosity, making it lightweight and suitable for packaging applications, while also providing a large surface area for antibacterial activity. Results demonstrated that this antibacterial pad exhibits an ultralow density of 9.0 mg/cm3 and an ultrahigh porosity of 99.10%. It can extend the shelf life of Channel Catfish fillets to 9 days at 4 °C, with a total volatile base nitrogen below 20 mg/100 g. The study proposes a novel solution for preserving aquatic products by combining antibacterial substances with the natural base material aerogel. This approach also extends the utilization of aerogel and nisin in food packaging.

Long-Term Triclocarban Exposure Induced Enterotoxicity by Triggering Intestinal AhR-Mediated Inflammation and Disrupting Microbial Community in Mice.

Exposure to triclocarban (TCC), a commonly used antibacterial agent, has been shown to induce significant intestine injuries and colonic inflammation in mice. However, the detailed mechanisms by which TCC exposure triggered enterotoxicity remain largely unclear. Herein, intestinal toxicity effects of long-term and chronic TCC exposure were investigated using a combination of histopathological assessments, metagenomics, targeted metabolomics, and biological assays. Mechanically, TCC exposure caused induction of intestinal aryl hydrocarbon receptor (AhR) and its transcriptional target cytochrome P4501A1 (Cyp1a1) leading to dysfunction of the gut barrier and disruption of the gut microbial community. A large number of lipopolysaccharides (LPS) are released from the gut lumen into blood circulation owing to the markedly increased permeability and gut leakage. Consequently, toll-like receptor-4 (TLR4) and NF-κB signaling pathways were activated by high levels of LPS. Simultaneously, classic macrophage phenotypes were switched by TCC, shown with marked upregulation of macrophage M1 and downregulation of macrophage M2 that was accompanied by striking upregulation of proinflammatory factors such as Il-1ß, Il-6, Il-17, and Tnf-α in the intestinal lamina propria. These findings provide new evidence for the TCC-induced enterotoxicity.

TP63 truncating mutation causes increased cell apoptosis and premature ovarian insufficiency by enhanced transcriptional activation of CLCA2.

BACKGROUND: Premature ovarian insufficiency (POI) is a severe disorder leading to female infertility. Genetic mutations are important factors causing POI. TP63-truncating mutation has been reported to cause POI by increasing germ cell apoptosis, however what factors mediate this apoptosis remains unclear. METHODS: Ninety-three patients with POI were recruited from Beijing Obstetrics and Gynecology Hospital, Capital Medical University. Whole-exome sequencing (WES) was performed for each patient. Sanger sequencing was used to confirm potential causative genetic variants. A minigene assay was performed to determine splicing effects of TP63 variants. A TP63-truncating plasmid was constructed. Real-time quantitative PCR, western blot analyses, dual luciferase reporter assays, immunofluorescence staining, and cell apoptosis assays were used to study the underlying mechanism of a TP63-truncating mutation causing POI. RESULTS: By WES of 93 sporadic patients with POI, we found a 14-bp deletion covering the splice site in the TP63 gene. A minigene assay demonstrated that the 14-bp deletion variant led to exon 13 skipping during TP63 mRNA splicing, resulting in the generation of a truncated TP63 protein (TP63-mut). Overexpression of TP63-mut accelerated cell apoptosis. Mechanistically, the TP63-mut protein could bind to the promoter region of CLCA2 and activate the transcription of CLCA2 several times compared to that of the TP63 wild-type protein. Silencing CLCA2 using a specific small interfering RNA (siRNA) or inhibiting the Ataxia Telangiectasia Mutated (ATM) pathway using the KU55933 inhibitor attenuated cell apoptosis caused by TP63-mut protein expression. CONCLUSION: Our findings revealed a crucial role for CLCA2 in mediating apoptosis in POI pathogenesis, and suggested that CLCA2 is a potential therapeutic target for POI.

Highly efficient and selective removal of anionic dyes from aqueous solutions using polyacrylamide/peach gum polysaccharide/attapulgite composite hydrogels with positively charged hybrid network.

To avoid the weakness (lower adsorption rate and selectivity) of peach gum polysaccharide (PGP) and improve the adsorption performance of polyacrylamide (PAAm) hydrogel (lower adsorption capacity), in the present work, the PGP was chemically tailored to afford ammoniated PGP (APGP) and quaternized PGP (QPGP), and attapulgite (ATP) was bi-functionalized with cation groups and carbon­carbon double bond. Then, PAAm/APGP and PAAm/QPGP/ATP hydrogels were synthesized via redox polymerization. The synthesis procedure and properties of hydrogels were traced by FTIR, SEM, XPS, TGA, TEM, and BET methods, and the dye adsorption performance of the hydrogels was evaluated using the new coccine (NC) and tartrazine (TTZ) aqueous solutions as the model anionic dyes. Effects of initial dye concentration, pH, and ionic strength on the adsorption were investigated. Compared with PAAm/APGP hydrogel, PAAm/APGP/ATP hydrogel exhibits higher adsorption rate, superior adsorption capacity, stability, and selectivity towards anionic dye. The adsorption process of PAAm/QPGP/ATP hydrogel reached equilibrium in about 20 min and followed the pseudo-second-order kinetic model and Langmuir isotherm. The adsorption capacities towards NC and TTZ of PAAm/QPGP/ATP hydrogel were calculated as 873.235 and 731.432 mg/g. This hydrogel adsorbent originating from PAAm, PGP, and ATP shows great promise for application in practical water treatment.

Thermo-sensitive hydroxybutyl chitosan/diatom biosilica hydrogel with immune microenvironment regulatory for chronic wound healing.

This study proposes a chronic wound therapeutic strategy based on extracellular matrix (ECM) biomimetics and immune regulation. The hydroxybutyl chitosan/diatom biosilica hydrogel (H/D) which can regulate the immune microenvironment, is prepared from hydroxybutyl chitosan (HBC) as matrix to construct the bionic ECM and diatom biosilica (DB) as structural active unit. The hierarchical porous structure of DB provides strong anchoring interface effect to enhance the mechanical strength of hydrogel, while maintaining its favorable temperature phase transition behavior, improving the material's fit to the wound and convenience of clinical use. Silicates released from DB in H/D accelerate the transition of wounds from inflammation to proliferation and remodeling. In cellular and diabetic rat models, H/D reduces inflammation (induces conversion of M1-type macrophages to M2-type), induces angiogenesis (1.96-fold of control), promotes fibroblast proliferation (180.36 % of control), collagen deposition, keratinocyte migration (47.34 % more than control), and re-epithelialization. This study validates a possible biological mechanism for H/D bioactive hydrogel-mediated regulation of the immune microenvironment and provides a simple synergistic dressing strategy.

The SGLT2 inhibitor empagliflozin attenuates atherosclerosis progression by inducing autophagy

Cardiovascular disease due to atherosclerosis is one of the leading causes of death worldwide; however, the underlying mechanism has yet to be defined. The sodium-dependent glucose transporter 2 inhibitor (SGLT2i) empagliflozin is a new type of hypoglycemic drug. Recent studies have shown that empagliflozin not only reduces high glucose levels but also exerts cardiovascular-protective effects and slows the process of atherosclerosis. The purpose of this study was to elucidate the mechanism by which empagliflozin ameliorates atherosclerosis. Male apolipoprotein E-deficient (ApoE−/−) mice were fed a high-fat Western diet to establish an atherosclerosis model. The area and size of atherosclerotic lesions in ApoE−/− mice were then assessed by performing hematoxylin–eosin (HE) staining after empagliflozin treatment. Concurrently, oxidized low-density lipoprotein (oxLDL) was used to mimic atherosclerosis in three different types of cells. Then, following empagliflozin treatment of macrophage cells (RAW264.7), human aortic smooth muscle cells (HASMCs), and human umbilical vein endothelial cells (HUVECs), western blotting was applied to measure the levels of autophagy-related proteins and proinflammatory cytokines, and green fluorescent protein (GFP)-light chain 3 (LC3) puncta were detected using confocal microscopy to confirm autophagosome formation. Oil Red O staining was performed to detect the foaming of macrophages and HASMCs, and flow cytometry was used for the cell cycle analysis. 5-ethynyl-2′-deoxyuridine (EdU), cell counting kit-8 (CCK-8), and scratch assays were also performed to examine the proliferation and migration of HASMCs. Empagliflozin suppressed the progression of atherosclerotic lesions in ApoE−/− mice... (AU)

The SGLT2 inhibitor empagliflozin attenuates atherosclerosis progression by inducing autophagy

Cardiovascular disease due to atherosclerosis is one of the leading causes of death worldwide; however, the underlying mechanism has yet to be defined. The sodium-dependent glucose transporter 2 inhibitor (SGLT2i) empagliflozin is a new type of hypoglycemic drug. Recent studies have shown that empagliflozin not only reduces high glucose levels but also exerts cardiovascular-protective effects and slows the process of atherosclerosis. The purpose of this study was to elucidate the mechanism by which empagliflozin ameliorates atherosclerosis. Male apolipoprotein E-deficient (ApoE−/−) mice were fed a high-fat Western diet to establish an atherosclerosis model. The area and size of atherosclerotic lesions in ApoE−/− mice were then assessed by performing hematoxylin–eosin (HE) staining after empagliflozin treatment. Concurrently, oxidized low-density lipoprotein (oxLDL) was used to mimic atherosclerosis in three different types of cells. Then, following empagliflozin treatment of macrophage cells (RAW264.7), human aortic smooth muscle cells (HASMCs), and human umbilical vein endothelial cells (HUVECs), western blotting was applied to measure the levels of autophagy-related proteins and proinflammatory cytokines, and green fluorescent protein (GFP)-light chain 3 (LC3) puncta were detected using confocal microscopy to confirm autophagosome formation. Oil Red O staining was performed to detect the foaming of macrophages and HASMCs, and flow cytometry was used for the cell cycle analysis. 5-ethynyl-2′-deoxyuridine (EdU), cell counting kit-8 (CCK-8), and scratch assays were also performed to examine the proliferation and migration of HASMCs. Empagliflozin suppressed the progression of atherosclerotic lesions in ApoE−/− mice... (AU)