Abstract:This article introduces the key updates of the “AHA/ACC/ESC/WHF Second Edition Expert Consensus Document on the Universal Definition of Heart Failure (2026)” and proposes Chinese translation recommendations for various definitions in the new consensus. The new consensus updates the classification of heart failure based on left ventricular ejection fraction (LVEF) as follows:(1) Heart failure with reduced ejection fraction (HFrEF), LVEF＜50%; (2) Heart failure with preserved ejection fraction (HFpEF), LVEF≥50%; (3) Heart failure with improved ejection fraction (HFimpEF); simultaneously, it also defines three stages in the treatment outcomes of heart failure patients:improved heart failure, remission heart failure, and recovery heart failure.

Abstract:The incidence and mortality of cardiovascular diseases (CVD) in China have been continuously rising, posing a serious threat to public health. Extensive studies have demonstrated the important value of carotid ultrasound in the prediction and diagnosis of cardiovascular risks. In recent years, artificial intelligence (AI) has rapidly advanced in the field of ultrasonic imaging, showing great promise in the intelligent identification of carotid plaques, extraction of vulnerable features and assessment of cardiovascular risk. This article systematically reviews the relevant literature to summarize the research progress of carotid ultrasound metrics from traditional imaging to the integration of AI technologies. Focusing on core metrics such as carotid intima-media thickness, plaque burden, vulnerability features, and hemodynamic parameters, it explores the correlation between these indicators and CVD. Furthermore, the review provides a comprehensive outlook on the advances and translational challenges of AI in this field, aiming to provide a theoretical basis and cutting-edge support for the early diagnosis and intervention of CVD.

Abstract:When long-term energy intake exceeds energy expenditure, obesity is induced. Energy expenditure driven by non-shivering thermogenesis is an important target for improving energy homeostasis and treating obesity. Brown adipose tissue (BAT) is the primary site of non-shivering thermogenesis, and its function is regulated by multiple systems through extracellular mechanisms. This review summarizes the extracellular regulatory mechanisms of BAT thermogenesis:the nervous system integrates cold and metabolic signals through the central-sympathetic neural axis, and hypothalamic neural circuits sense lipid and hormonal states to dynamically adjust BAT thermogenic thresholds. In the immune system, macrophages participate in metabolic regulation through polarization dynamics, secretome remodeling and mitochondrial transfer, while mast cells and T cell subsets bidirectionally regulate the BAT microenvironment through cytokine networks.The digestive system influences BAT thermogenesis through gastrointestinal hormones (secretin, bile acids, cholecystokinin, glucagon-like peptide-1 (GLP-1), etc.), liver-secreted proteins (pregnancy zone protein(PZP), fibroblast growth factor 21 (FGF21) and metabolites, as well as gut microbiota-derived metabolites (short-chain fatty acids, bile acids). In autocrine and paracrine mechanisms, BAT performs local regulation by secreting myostatin, irisin, mitochondrial extracellular vesicle, vascular endothelial growth factor-α (VEGF-α), fibroblast growth factor 21 (FGF21), and neuregulin 4. Additionally, BAT activation can delay atherosclerosis progression through mechanisms including lipid clearance, anti-inflammatory effects, and adipokine secretion. This review systematically outlines the extracellular regulatory network of BAT thermogenesis, providing a theoretical foundation and potential intervention targets for the prevention and treatment of metabolic diseases.

Abstract:Aim To investigate whether sphingosine-1-phosphate (S1P) promotes LC3-associated phagocytosis via its receptor S1PR1, thereby enhancing the efferocytosis of THP-1-derived macrophages. Methods THP-1 monocytes were induced to differentiate into macrophages using 80 μg/L phorbol ester; 254 nm ultraviolet radiation was used to induce early apoptosis in Jurkat cells for cell phagocytosis experiments. Macrophages were treated with 0,0.5,1.0 and 1.5 μmol/L S1P for 12 h, or treated with 1.5 μmol/L S1P alone or in combination with S1PR1 antagonist W146, S1PR2 antagonist JTE-013, S1PR3 antagonist CAY10444 and ATG4B inhibitor NSC185058. Western blot was used to detect the expression levels of MerTK, Axl, Tyro3, LC3B and LAMP1, fluorescence-labeled apoptotic cells were applied in phagocytosis assays to evaluate phagocytic efficiency, ELISA was employed to measure the levels of pro-inflammatory factors (TNF-α, IL-6 and IL-1β) and anti-inflammatory factors (TGF-β, IL-4 and IL-10) in the supernatant. Results S1P could significantly enhance the phagocytic capacity of macrophages for apoptotic cells, and this effect was concentration-dependent. Specifically, the phagocytic efficiency of macrophages for apoptotic cells was significantly improved (P＜0.01); the expression of cell burial receptors MerTK, Axl and Tyro3 was markedly upregulated (P＜0.01); at the same time, levels of anti-inflammatory factors (TGF-β, IL-4 and IL-10) increased (P＜0.01), while pro-inflammatory factors (TNF-α, IL-6 and IL-1β) decreased (P＜0.01). The results of the S1P blockade experiment showed that blocking S1PR1 with W146 could reverse the efferocytosis of S1P (P＜0.05), while blocking S1PR2 or S1PR3 had no significant effect. S1P treatment significantly increased the gene and protein expression levels of LC3B and LAMP1 in macrophages (P＜0.01) and promoted lysosome maturation. After NSC185058 treatment, the phagocytic efficiency and anti-inflammatory factor secretion of macrophages decreased (P＜0.05). In addition, the inhibitory effect of blocking S1PR1 and LC3-related phagocytosis on efferocytosis was more significant (P＜0.01). Conclusion S1P significantly enhances the phagocytic clearance ability of THP-1-derived macrophages towards apoptotic cells through S1PR1-mediated LC3-related phagocytosis, and promotes the transformation of macrophages into anti-inflammatory phenotypes.

Abstract:Aim To investigate the effect of membrane-bound O-acyltransferase domain-containing 2 (MBOAT2) on mitophagy in vascular endothelial cells and its mechanisms. Methods Western blot was used to detect MBOAT2 protein expression in human atherosclerotic plaques. A human umbilical vein endothelial cell model with MBOAT2 overexpression was established. Western blot, transmission electron microscopy, JC-1 staining, MitoSOX Red staining, mRFP-GFP-LC3 dual-fluorescence staining and immunofluorescence staining were employed to assess the effects of MBOAT2 overexpression on mitochondrial injury, mitophagy, cytosolic mtDNA release, and activation of the cyclic GMP-AMP synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway. In addition, the cGAS specific inhibitor RU.521 was used for intervention to verify the role of the cGAS-STING signaling pathway in mitochondrial injury and mitophagy dysfuntion. Results Compared with the control group, the expression of MBOAT2 protein in human atherosclerotic plaques increased by 70.7% (P＜0.05). After overexpression of MBOAT2, the expression levels of MIC60, ATP5L and ATP5I in human umbilical vein endothelial cells were downregulated by 15.6%, 18.9% and 25.8%, respectively (P＜0.05 or P＜0.01), accompanied by abnormal mitochondrial ultrastructure, decreased membrane potential and increased mitochondrial reactive oxygen species (mtROS); the expression levels of PINK1, Parkin, LC3Ⅱ and p62 proteins increased by 53.7%, 53.8%, 54.9% and 112.1%, respectively (P＜0.05 or P＜0.01), and the number of yellow autophagosomes and red autolysosomes increased; in addition, the expression level of cGAS protein increased by 121%, the phosphorylation level of TANK-binding kinase 1 (TBK1) increased by 52.5% (P＜0.05 or P＜0.01), and the release of mtDNA into the cytoplasm was observed. Compared with the MBOAT2 overexpression group, after RU.521 intervention, the expression level of cGAS protein decreased by 58.4% and the phosphorylation level of TBK1 decreased by 64.7%; PINK1, Parkin, LC3Ⅱ/LC3Ⅰ ratio and p62 decreased by 44.1%, 53.4%, 44.7% and 65.0%, respectively (P＜0.05 or P＜0.01). At the same time, the number of yellow autophagosomes and red autolysosomes decreased, the level of mtROS decreased, and the damage to mitochondrial cristae structure was alleviated. Conclusion MBOAT2 induces mitophagy dysfunction in vascular endothelial cells, thereby activating the mtDNA-cGAS-STING signaling pathway.

Abstract:Aim To explore the antagonistic effect of sesamol on endothelial cell injury induced by oxidized low density lipoprotein (ox-LDL), and elucidate its molecular mechanism of exerting antioxidant stress, inhibiting abnormal angiogenesis and blocking endothelial-to-mesenchymal transition (EndMT) through the JNK/Nrf2/HO-1 pathway. Methods Human umbilical vein endothelial cells and human aortic endothelial cells were used to establish an endothelial cell injury model induced by 75 μmol/L ox-LDL. The CCK-8 method, DCFH-DA fluorescent probe and Annexin V/PI apoptosis detection method were used to evaluate the safety of sesamol and its effects on cell viability, as well as its protective effects against oxidative stress and cell apoptosis; Matrigel tubular formation experiment, Transwell migration/invasion experiment RT-qPCR, immunofluorescence and Western blot techniques were used to detect the effects of sesamol on abnormal angiogenesis, endothelial barrier function and EndMT; time gradient Western blot, JNK inhibitor SP600125 intervention and immunofluorescence experiments were used to verify the activation and necessity of the JNK/Nrf2/HO-1 pathway. Results The oxidative stress model of endothelial cells was successfully established by stimulating with 75 μmol/L ox-LDL for 24 hours, which showed a significant increase in reactive oxygen species (ROS) levels, upregulation of inflammation/adhesion molecule expression, downregulation of endothelial nitric oxide synthase (eNOS) and vascular endothelial cadherin expression, and an increase in cell apoptosis rate (P＜0.05 or P＜0.01). Sesamol (≤ 50 μmol/L) was non-toxic to normal endothelial cells; among them, 50 μmol/L sesamol could significantly restore the decrease in cell viability induced by ox-LDL, inhibit ROS generation and cell apoptosis (P＜0.05 or P＜0.01); simultaneously, it could significantly inhibit the formation of abnormal tube braching points and cell migration, downregulate the expression of vascular endothelial growth factor/vascular endothelial growth factor receptor 2 and matrix metalloproteinase-9, upregulate the expression of zonula occludens-1, claudin-5, and VE-cadherin, and restore nitric oxide production (P＜0.05 or P＜0.01); in addition, this concentration of sesamol could reverse EndMT-related phenotypes, reduce the expression of mesenchymal markers such as α-smooth muscle actin and vimentin, and restore the expression levels of CD31 and VE-cadherin (P＜0.05 or P＜0.01). Mechanism studies showed that sesamol could time-dependently activate the expression of p-JNK, nuclear Nrf2, and downstream HO-1 (P＜0.01); the JNK inhibitor SP600125 could block the nuclear translocation of Nrf2 and inhibit the protective effect of sesamin (P＜0.01). Conclusion Sesamol can significantly antagonize the injury of vascular endothelial cells induced by ox-LDL, and its mechanism is related to the activation of JNK/Nrf2/HO-1 pathway, inhibition of oxidative stress, abnormal angiogenesis and EndMT induced by ox-LDL, which provides an important experimental basis for its use as a potential natural drug to prevent and treat atherosclerosis.

Abstract:Aim To evaluate the value of the monocyte-to-high density lipoprotein cholesterol ratio (MHR) combined with systemic inflammation response index (SIRI) in predicting the risk of heart failure (HF) readmission in elderly patients with type 2 diabetes mellitus (T2DM) and acute coronary syndrome (ACS), and to establish a risk prediction model. Methods In this retrospective cohort study, 775 elderly inpatients with T2DM and ACS hospitalized in the Affiliated Hospital of Inner Mongolia Medical University from January 2023 to October 2025 were enrolled. The primary endpoint was the first readmission for HF in our hospital from discharge to the data cutoff date. All patients were randomly divided into a training set (n＝542) and a test set (n＝233) at a ratio of 7∶3. LASSO regression followed by multivariate Logistic regression was used to identify independent predictors and construct the prediction model. Model performance was assessed using receiver operating characteristic (ROC) curves, calibration curves, and decision curve analysis, and a nomogram was established. The SHAP method was used to quantify the contribution of each predictor to the model. Results A total of nine independent predictors were identified:sex, history of primary stent implantation, history of secondary stent implantation, platelet count (PLT), low density lipoprotein cholesterol (LDLC), globulin (Glo), left ventricular ejection fraction (LVEF), MHR and SIRI. Multivariate Logistic regression showed that higher MHR (OR＝4.4,5%CI:2.972～6.704, P＜0.001) and higher SIRI (OR＝1.0,5%CI:1.015～1.823, P＝0.039) were independently associated with an increased risk of HF readmission, whereas higher LVEF (OR＝0.0,5%CI:0.233～0.439, P＜0.001) was independently associated with a reduced risk of HF readmission. In the test set, the Logistic regression model achieved an area under the curve (AUC) of 0.917, demonstrating good discrimination and calibration. SHAP analysis showed that MHR contributed most to the model prediction, followed by LVEF. ConclusionMHR combined with SIRI effectively predicts the risk of HF readmission in elderly patients with T2DM and ACS. The Logistic regression-based nomogram showed good predictive performance and potential clinical utility.

Abstract:Aim To construct and validate a predictive nomogram model for the risk of postoperative stroke. Methods We retrospectively enrolled 358 surgical patients who developed stroke between July 2017 and August 2023 at the Affiliated Hospital of Jining Medical University, and matched them 1∶2 with 714 contemporaneous surgical patients without postoperative stroke. Using R software, the cohort was randomly split into a training set (n＝751) and a validation set (n＝321) in a 7∶3 ratio. Significant variables in univariate Logistic regression were included in Lasso regression to determine independent predictors, which were then used to build a nomogram model for postoperative stroke risk. Discrimination and calibration were assessed with ROC curves and calibration plots, respectively; decision-curve analysis was used to evaluate clinical utility and net benefit. Results Except for age and total bilirubin, baseline clinical data were comparable between the training and validation sets (P＞0.05). Lasso regression revealed history of cerebral infarction, preoperative VTE score, serum albumin and plasma fibrinogen as independent predictors of postoperative stroke. A nomogram model incorporating these factors was constructed. The area under the ROC curve was 0.651 in the training set and 0.683 in the validation set. Calibration plots demonstrated high agreement between predicted and observed probabilities.Decision-curve analysis indicated favorable net benefit within a risk threshold probability range of 0～0.61. Conclusion History of cerebral infarction, high risk of preoperative VTE score, decreased albumin, and increased plasma fibrinogen are related to the risk of postoperative stroke. The constructed nomogram model can effectively predict the prognosis of patients.

Abstract:Aim To explore the correlation between postoperative serum nuclear factor-κB (NF-κB) level changes and early aortic adverse events (AAE) as well as its predictive value in patients with Stanford type B traumatic aortic dissection (TBAD), so as to provide a theoretical basis for early clinical identification of postoperative AAE risk. Methods A total of 159 patients with TBAD admitted to our hospital from April 2021 to August 2024 were retrospectively enrolled, and 146 patients were finally included according to the inclusion and exclusion criteria. All patients were divided into AAE group (n＝47) and non-AAE group (n＝99) based on the occurrence of postoperative AAE. Meanwhile, 150 cases were randomly selected via the random number table method from 364 patients with non-traumatic aortic dissection receiving thoracic endovascular aortic repair, who were assigned to the non-TBAD group. Repeated-measures analysis of variance was used to compare NF-κB levels before surgery, 1 month and 3 months after surgery. Dose-response plots were generated to analyze the correlation between the reduction in NF-κB levels (ΔNF-κB) and the probability of false lumen thrombosis. A generalized linear mixed model (GLMM) was employed to analyze the correlation between ΔNF-κB and the risk of AAE. ROC curves were used to evaluate the predictive performance of ΔNF-κB for AAE. Restricted cubic spline (RCS) models were used to analyze the association between ΔNF-κB and AAE risk. The R package Interplot was used to generate interaction plots of ΔNF-κB with false lumen thrombosis degree on AAE risk. The Kaplan-Meier method was used to plot survival curves to evaluate the occurrence of AAE in patients with different levels of ΔNF-κB. Results The 1-month postoperative NF-κB decreased level (ΔNF-κB₁) in the AAE group was 0.69-fold and 0.76-fold that of the non-TBAD and non-AAE groups, respectively, while the 3-month postoperative decreased level (ΔNF-κB₂) was 0.74-fold and 0.80-fold, respectively (P＜0.05). The dose-dependent plot results showed that the probability of false lumen thrombosis formation gradually increased with the elevation of ΔNF-κB₁ and ΔNF-κB₂ in the AAE group, and tended to stabilize when ΔNF-κB₁＞0.62 μg/L or ΔNF-κB₂＞0.69 μg/L. GLMM analysis showed that compared with ΔNF-κB₁＜0.15 μg/L, ΔNF-κB₁＜0.56 μg/L was positively associated with AAE risk, and ΔNF-κB₁≥0.56 μg/L was negatively associated with AAE risk (P＜0.05). Compared with ΔNF-κB₂＜0.18 μg/L, ΔNF-κB₂＜0.66 μg/L was positively correlated with AAE risk, and ΔNF-κB₂≥0.66 μg/L was negatively correlated with AAE risk. ROC analysis showed that the AUC of ΔNF-κB₁ for predicting AAE was 0.784 (95%CI:0.710～0.859, P＜0.001), and the best cut-off value was 0.62 μg/L; the AUC of ΔNF-κB₂ for predicting AAE was 0.811 (95%CI:0.741～0.881, P＜0.001), and the best cut-off value was 0.69 μg/L, suggesting that ΔNF-κB₂ had a stronger predictive performance for AAE. RCS model analysis showed that with the increase of ΔNF-κB₁ and ΔNF-κB₂, the risk of AAE showed a decreasing trend (P＜0.05). The interaction diagram showed that the negative correlation between false lumen thrombosis degree and AAE risk was enhanced along with the increase of NF-κB reduction magnitude. The Kaplan-Meier survival curve showed that there was a statistically significant difference in the incidence of AAE among patients with different levels of ΔNF-κB₁ and ΔNF-κB₂ (χ²＝5.064, P＝0.028), and patients with higher ΔNF-κB levels had a lower incidence of AAE. Conclusion Postoperative reduction of serum NF-κB level can effectively predict the risk of early AAE in TBAD patients, which is negatively correlated with the AAE risk, and this mechanism may be mediated by promoting false lumen thrombosis.

Abstract:Aim To investigate the effects of proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors on the incidence of restenosis 1 year and major adverse cardiovascular and cerebrovascular events (MACCE) 3 years after percutaneous coronary intervention (PCI) in elderly patients with diabetes and acute coronary syndrome (ACS). Methods 320 elderly patients with diabetes and ACS were randomly divided into the conventional treatment group and PCSK9 inhibitor group, with 160 cases in each group. The conventional treatment group received standardized drug treatment after PCI, while the PCSK9 inhibitor group received PCSK9 inhibitor in addition to standardized drug treatment for a course of 1 year. The total cholesterol (TC), triglyceride (TG), high density lipoprotein cholesterol (HDLC), low density lipoprotein cholesterol (LDLC), lipoprotein (a), high sensitivity C-reactive protein (hs-CRP), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and other test indicators as well as the incidence of restenosis at PCI site were observed in the two groups of patients, and the primary endpoint (myocardial infarction, cardiac death, and all-cause death), the composite endpoint (myocardial infarction, cardiac death, ischemia-driven repeat revascularization, stent thrombosis, and stroke) of the secondary endpoint (MACCE) and the incidence of angina pectoris and hospital readmission were comparatively analyzed through 3-year follow-up. Results After 1 year of treatment, the levels of TC, TG, LDLC, lipoprotein (a), hs-CRP, TNF-α, IL-6, and the incidence of restenosis in the PCSK9 inhibitor group were significantly lower than those in the conventional treatment group (P＜0.05). The 3-year follow-up results showed that the primary endpoint events (cardiac death, myocardial infarction), total MACCE, stent thrombosis, angina recurrence, and repeat revascularization incidence in the PCSK9 inhibitor group were significantly lower than those in the conventional treatment group (P＜0.05). Conclusion PCSK9 inhibitors can effectively reduce the blood lipid level, inhibit inflammatory reaction, and reduce the incidence of restenosis 1 year after PCI and MACCE 3 years after PCI in elderly patients with diabetes and ACS.

Abstract:Aim To observe the incidence of major adverse cardiovascular events (ACE) during treatment with lorlatinib, a novel third-generation anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor (TKI), in patients with non-small cell lung cancer (NSCLC), and evaluate the effect of pharmacological interventions. Methods A total of 92 ALK-positive NSCLC patients admitted to Guangdong Provincial People's Hospital between March 2018 and January 2025 were selected. The study analyzed the incidence of ACE following lorlatinib treatment, including the immediate and long-term effects, and evaluated the effectiveness of statin intervention for hyperlipidemia induced by the treatment. Results A total of 92 ALK-positive NSCLC patients were included in the study. Hyperlipidemia was the most common ACE, observed in 59 patients (64.1%), with 1st, 2nd, and 3rd grade events occurring in 15 patients (25.4%), 33 patients (55.9%), and 11 patients (18.6%), respectively. No grade 4 events were reported. The CVAEs related to lorlatinib were concentrated in the early phase of treatment (0~6 months), particularly hyperlipidemia and sinus tachycardia. After 12 months of treatment, pericardial effusion and thrombosis still showed a certain incidence, suggesting that these cardiovascular events may have a long-term impact on patients' health. Statin intervention significantly mitigated dyslipidemia. Compared with the lorlatinib monotherapy group, the levels of total cholesterol (TC), triglycerides (TG), and low density lipoprotein (LDL) in the intervention group were significantly reduced by 35.25%, 64.15%, and 35.71%, respectively (P＜0.05). Conclusion Lorlatinib treatment for ALK-positive NSCLC patients demonstrated good efficacy, but its ACEs, especially hyperlipidemia and sinus tachycardia, require attention in clinical practice. Pharmacological interventions, particularly statins, can effectively control lipid levels, thereby reducing cardiovascular risks and improving patients' prognosis. Therefore, it is recommended to enhance early screening and close monitoring for high-risk patients in clinical practice, especially during the early stages of treatment, to ensure timely intervention and continuous attention to long-term adverse effects.

Abstract:Atherosclerosis(As), a chronic inflammatory pathological lesion, is the main cause of cardiovascular diseases(CVD) such as coronary heart disease, posing a serious threat to human health. Inflammatory reaction runs through the entire pathological progression of As, and exploring anti-atherosclerosis strategies from the anti-inflammatory perspective is of important significance. In recent years, Simiao Yong'an decoction and its components have been proven to exert multiple pharmacological effects such as anti-inflammation, lipid regulation and vascular endothelial protection. Starting from the inflammatory theory, this paper systematically summarizes the modern mechanism of Simiao Yong'an decoction and its components against As via regulating inflammation through multiple signaling pathways, so as to provide a theoretical reference for its application in the prevention and treatment of As.

Abstract:Coronary heart disease (CHD) is a common and frequently occurring cardiovascular disease in China, with atherosclerosis serving as its core pathological basis. As a chronic inflammatory immune response process, atherosclerosis plays a critical role in the initiation and progression of CHD. Therefore, investigating the mechanisms by which the immune system contributes to the development and progression of CHD has become a research hotspot in this field. This article reviews the research progress on T cells and their T-cell receptor (TCR) repertoire characteristics in CHD, including the roles of T cell subsets in CHD, as well as the diversity and specificity of the TCR repertoires, aiming to provide a theoretical basis for developing novel diagnostic tools and therapeutic strategies for CHD.