Abstract:Aortic dissection (AD) is a life-threatening acute vascular disease with a complex and not yet fully understood pathogenesis. In recent years, metabolic reprogramming has gradually emerged as a significant factor in the occurrence and development of AD. This review summarizes the abnormal alterations in major metabolic pathways, including amino acid metabolism, glucose metabolism, and lipid metabolism, and their impact on vascular cell functions in AD. Metabolic reprogramming contributes to the progression of AD by regulating the functions of endothelial cells (EC) and vascular smooth muscle cells (VSMC), thereby promoting the destruction of the vascular wall structure and exacerbating inflammatory responses. Additionally, this paper summarizes the potential applications of metabolism-related molecules in the early diagnosis and treatment of AD, emphasizing the importance of metabolic regulation as a novel strategy for AD prevention and management. Finally, future research directions in the study of metabolic reprogramming in AD are proposed, including in-depth mechanistic studies, the development of novel biomarkers, and the optimization of clinical intervention strategies, aiming to provide new insights and methods for the prevention and treatment of AD.

Abstract:Aim To investigate the clinical characteristics and related factors of post-implantation syndrome (PIS) following the prophylactic application of non-steroidal anti-inflammatory drugs (NSAID) after thoracic endovascular aortic repair (TEVAR). Methods A total of 510 adult patients who had received prophylactic NSAID after TEVAR at General Hospital of Northern Theater Command from September 2013 to April 2024 were consecutively included in the study. The patients were divided into two groups based on the occurrence of PIS postoperatively:the PIS group (34 patients, 6.67%) and the non-PIS group (476 patients, 93.33%). General information, past medical history and surgical features were compared between the two groups. Univariate and multivariate Logistic regression analysis were used to identify predictors of PIS. The ROC curve was used to assess the overall diagnostic performance of the risk factors. Results The baseline data and clinical characteristics of PIS group and non-PIS group were compared. The rate of gender as male, chest and back pain on adimission, limb ischaemia on admission, systolic blood pressure on admission, use of angiotensin converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB) drugs during hospitalization, preoperative white blood cell (WBC) count and surgical approach involving an incision in PIS group were higher than those in non-PIS group , and the age, preoperative estimated glomerular filtration rate (eGFR) level and use of statin drugs during hospitalization were lower than those in non-PIS group, all differences were statistically significant. Postoperative C-reactive protein level, incidence of clinical adverse events during postoperative hospitalization, and time of postoperative hospitalization were increased in PIS group compared with those in non-PIS group. There was no significant difference in the incidence of aortic adverse events between the two groups (P＜0.05). Univariate and multivariate Logistic regression analysis identified patients' age ＜ 60 years (OR＝4.1,5%CI:1.348~16.188, P＝0.015), increased preoperative WBC count (OR＝3.2,5%CI:1.469~8.735, P＝0.005), and surgical approach involving an incision (OR＝8.9,5%CI:1.849~37.610, P＝0.006) as independent predictors for PIS. The results of the ROC curve analysis showed that the area under the curve of patients' age ＜60 years, increased preoperative WBC count, femoral arteriotomy access, and the three combined diagnoses in predicting the occurrence of PIS after TEVAR were 0.653 (95%CI:0.573~0.733), 0.686(95%CI:0.600~0.771), 0.699(95%CI:0.627~0.770), 0.826(95%CI:0.765~0.887). Conclusion Despite the prophylactic use of NSAID, some patients develop PIS after TEVAR. Patients'age ＜ 60 years, elevated preoperative WBC count, and femoral artery incision approach are independent risk factors for PIS after preventive medication. Additionally, the incidence of PIS increased with the number of independent risk factors present.

Abstract:Aortic aneurysm (AA) and aortic dissection (AD) are critical cardiovascular disease emergencies that seriously threaten human life and health. Due to various factors, the progressive reduction of various types of cells, such as smooth muscle cells and endothelial cells in the aortic wall, is an essential mechanism for developing AA and AD. On this basis, AD is induced by mechanical stresses such as hypertension, leading to damaged endothelial rupture or hemorrhage within the aortic wall. However, AA causes the aortic wall to thin and expand outward in response to stimuli such as prolonged blood flow impingement. At present, increasing evidence shows that various programmed cell death, such as apoptosis, necroptosis, pyroptosis, ferroptosis, copper death, poly ADP-ribose polymerase 1 (PARP-1)-dependent cell death, and immunogenic cell death, play essential roles in the pathogenesis of AA and AD. Therefore, understanding the key molecules and pathways in the pathogenesis of AA and AD from the perspective of programmed cell death and searching for inhibitors of various types of programmed death is essential to prevent aortic destruction and disease progression. The review summarizes the roles and research progress of different types of programmed cell death modalities in the development of AA and AD, clarifies the central position of programmed cell death in forming AA and AD, and searches for new therapeutic methods for the clinic.

Abstract:Abdominal aortic aneurysm (AAA) is characterized by a localized and irreversible enlargement of the abdominal aorta, which poses a significant risk to life in the event of rupture. Currently, the primary treatment for AAA is surgical intervention, as there are no effective pharmacological therapies available to prevent or slow postoperative vascular dilation. Therefore, understanding the detailed pathogenesis of AAA and identifying effective prevention and treatment strategies is essential. This review begins by examining the pathological and molecular mechanisms involved in AAA, focusing on key research areas such as the phenotypic switching of vascular smooth muscle cells, inflammation and metabolic reprogramming. Based on a large of animal and clinical studies, this review then explores therapeutic strategies and promising drugs for AAA, including mesenchymal stem cell therapy, nanomaterial applications, and immunomodulatory interventions. The review aims to provide researchers with new ideas and directions for the prevention and treatment of AAA.

Abstract:Aim To investigate whether adipose differentiation-related proteins promote macrophage lipid accumulation by upregulating acyl-CoA synthetase long-chain family member 3 (ACSL3) expression through PI3K/Akt. Methods The experiments were divided into 24 h group, different PLIN2 expression groups, HA-PLIN2＋SC97 group and HA-PLIN2＋LY294002 group. Western blot was used to detect the protein expression of PLIN2, Akt, p-Akt and ACSL3 in cells, RT-qPCR was used to detect the mRNA level of PLIN2 in cells, and oil red O was used to observe the degree of lipid accumulation in cells. Results The protein expression levels of Akt, p-Akt and ACSL3 in macrophages overexpressing PLIN2 were significantly increased (P＜0.05), and p-Akt nuclear translocation was increased, with fluorescence labeling of PLIN2 and Akt overlapping. After adding the PI3K/Akt agonist SC97 to macrophages overexpressing PLIN2, the expression level of ACSL3 significantly increased (P＜0.05), and the degree of intracellular lipid accumulation increased; After adding the PI3K/Akt inhibitor LY294002 to macrophages overexpressing PLIN2, the expression level of ACSL3 significantly decreased (P＜0.05), and the degree of intracellular lipid accumulation decreased. Conclusion PLIN2 upregulates ACSL3 expression through PI3K/Akt, thereby promoting macrophage lipid accumulation.

Abstract:Aim To investigate the effect of irisin on endothelial inflammation and atherosclerosis (As) in mice. Methods ApoE－/－ mice were randomly divided into control group, As model group, and irisin group (treated with irisin based on the As model), with 10 mice in each group. The carotid tissues were stained using pathological techniques and immunofluorescence. Human aortic endothelial cells (HAEC) were cultured in vitro, treated with irisin, and stimulated with cholesterol crystal (CC). The protein levels of vascular cell adhesion molecule-1(VCAM-1) and intercellular cell adhesion molecule-1(ICAM-1) were then detected by Western blot. The expression of inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6) and chemokine (C-C motif) ligand 2 (CCL2) were detected by RT-qPCR. The adhesion of monocytes was assessed using cell adhesion assay. Results The carotid plaque area in the mice of As model group was significantly increased compared with that in control group (P＜0.05). In contrast, the plaque area was reduced in the irisin group compared with the As model group (P＜0.05). Compared with the control group, the expression of VCAM-1, the number of CD68＋ macrophages, and the deposition of CC were increased in the carotid arteries of the As model group (P＜0.05), while irisin could reduce the expression of VCAM-1, the number of CD68＋ macrophages, and the deposition of CC (P＜0.05). At the in vitro level, the expression of VCAM-1 and ICAM-1, as well as the adhesion of monocytes in CC-stimulated HAEC, were increased (P＜0.05). However, irisin could inhibit the increased expression of VCAM-1 and ICAM-1 (P＜0.05), as well as the adhesion of monocytes induced by CC (P＜0.05). The mRNA levels of IL-1β, IL-6 and CCL2 in HAEC of CC stimulated group were increased (P＜0.05), while irisin could inhibit the mRNA expressions of IL-1β, IL-6 and CCL2 induced by CC (P＜0.05). Conclusion Irisin can inhibit vascular inflammation, thereby reducing the occurrence and progression of atherosclerosis.

Abstract:Aim To investigate the regulatory effects of coenzyme Q10 (CoQ10) on blood lipid level and intestinal flora abundance in atherosclerotic (As) rats. Methods 24 rats were randomly divided into control group, As group and CoQ10 intervention group. Rats in the As group and CoQ10 intervention group were fed with high-fat chow for 2 weeks, combined with abdominal aortic balloon injury to replicate the As model. CoQ10 was administered by gavage starting on the next day of modeling, once daily for 4 weeks. Aortic Movat's staining and lipid levels were used to verify the effect of CoQ10 intervention in As, and the abundance of intestinal flora in intestinal contents was analyzed using metagenomics. Results Compared with the control group, rat aortic tissues in the As group showed endothelial damage, structural disorganization of the internal elastic plate and inflammatory infiltration, serum triglyceride (TG), total cholesterol (TC) and low density lipoprotein cholesterol (LDLC) levels were increased, and high density lipoprotein cholesterol (HDLC) levels were decreased. Compared with the As group, the structure of the endothelial cells of the aorta and the structure of the endothelial cells, the internal elastic plates and the smooth muscle cell morphology were relatively regular, serum TC, TG and LDLC levels were decreased, and HDLC levels were increased in the CoQ10 intervention group. Compared with the control group, the intestinal bacterial biodiversity in the As group was reduced. At the phylum level, the abundance of the Firmicutes and the Bacteroidetes were down-regulated, whereas that of Proteobacteria was up-regulated. At the genus level, the relative abundance of Lactobacillus, Bacteroides, Akkermansia, Limosilactobacillus, Parabacteroides and Ligilactobacillus was down-regulated, and the relative abundance of Muribaculum was up-regulated. Compared with the As group, CoQ10 intervention restored the biodiversity of the intestinal microbiota in As rats and increased the relative abundance of Firmicutes, Bacteroidetes, Lactobacillus, Bacteroides, Akkermansia, Limosilactobacillus, Parabacteroides and Ligilactobacillus, while reducing the relative abundance of Proteobacteria and Muribaculum (all P＜0.05). ConclusionCoQ10 can regulate blood lipid levels in As rats, upregulate the abundance of beneficial microbiota, downregulate the abundance of harmful microbiota, and modulate the diversity of the gut microbiota.

Abstract:Aim To explore the safety and efficacy of simple drug-coated balloon (DCB) compared with provisional stenting (PS) in the treatment of pseudo-left main (pseudo-LM) bifurcation lesions. Methods A retrospective analysis was performed on 175 patients who underwent coronary angiography for pseudo-LM bifurcation lesions and interventional treatment at the Second Affiliated Hospital of Zhengzhou University from January 2018 to January 2023. According to the treatment strategy, they were divided into drug-eluting stent (DES) group (99 cases) and DCB group (76 cases).Preoperative and immediate postoperative quantitative coronary angiography (QCA) data were recorded, and patients were followed up. The follow-up endpoints included the occurrence of major adverse cardiovascular events (MACE) and hospital re-admission. Coronary angiography and QCA data during follow-up were also recorded. Results The immediate postoperative minimum lumen diameter and lumen gain in the left main (LM), left anterior descending (LAD), and left circumflex (LCX) arteries of the DCB group were smaller than those of the DES group (P＜0.05), while the degree of residual lumen stenosis immediately after surgery was greater than that of the DES group (P＜0.05). QCA was performed on the coronary angiography results of follow-up patients. The minimum lumen diameter in LM, LAD, and LCX was smaller in the DCB group than in the DES group during follow-up (P＜0.05). The degree of residual lumen stenosis during follow-up was greater in the DCB group than in the DES group (P＜0.05), but the late lumen loss in LM, LAD, and LCX was smaller in the DCB group than that in the DES group, with statistically significant differences (P＜0.05). There was no significant difference in the incidence of postoperative MACE between the two groups during the follow-up period (P＞0.05). Cox regression analysis showed that the choice of interventional treatment (DCB vs. PS) had no significant impact on the risk of MACE (P＞0.05). Conclusion Compared with PS, DCB alone demonstrates relatively satisfactory efficacy and safety in the treatment of pseudo-LM bifurcation lesions and can be considered as an alternative treatment strategy for interventional therapy of such lesions.

Abstract:Aim To analyze the correlation between serum retinol-binding protein 4 (RBP4), low density lipoprotein cholesterol to albumin ratio (LDLC/Alb), monocyte to high density lipoprotein ratio (MHR) and plaque stability in carotid atherosclerosis population and their predictive value for acute ischemic stroke (AIS). Methods A total of 197 patients with asymptomatic carotid atherosclerosis admitted to our hospital from September 2021 to January 2023 were selected for a prospective cohort study, and they were categorized into occurred group and non-occurred group according to whether AIS occurred within 12 months. Baseline information at time of visit, results of the cervical ultrasonography and serum RBP4, LDLC/Alb, MHR levels were compared between the two groups. Spearman/Pearson and receiver operating characteristic (ROC) curve were used to analyze the correlation of RBP4, LDLC/Alb and MHR with carotid atherosclerosis and plaque stability, and the value of predicting AIS in carotid atherosclerosis population. Hosmer-Lemeshow goodness of fit test was used to evaluate the calibration ability of serum RBP4, LDLC/Alb and MHR to jointly predict AIS in carotid atherosclerosis population. Results The carotid intima-media thickness (IMT) was higher in occurred group than that in non-occurred group. There were more soft plaques and mixed plaques in occurred group than in non-occurred group (P＜0.05). Serum levels of RBP4, LDLC/Alb and MHR were higher in occurred group than those in non-occurred group (P＜0.05). The correlation analysis showed that the levels of serum RBP4, LDLC/Alb and MHR were positively correlated with IMT (r＝0.3,0.0,0.710) and plaque properties (r＝0.6,0.5,0.703) (P＜0.001). ROC curve analysis showed that the AUC of serum RBP4, LDLC/Alb and MHR in predicting AIS in carotid atherosclerosis population was 0.6,0.821 and 0.828, respectively, and the AUC of MHR was the largest; the AUC of the combination of serum RBP4, LDLC/Alb and MHR was 0.936, which was higher than that of MHR (Z＝2.978, P＜0.05), the predictive sensitivity and specificity were 88.24% and 87.40%. Hosmer-Lemeshow goodness of fit test showed that there was no significant difference between serum RBP4, LDLC/Alb and MHR in predicting AIS and the actual observation value in carotid atherosclerosis population (P＞0.05), and the prediction model had good calibration ability. Conclusion Serum RBP4, LDLC/Alb, and MHR are positively correlated with carotid atherosclerosis and plaque stability, and can predict the occurrence of AIS. Combined detection of the three can be used as a method for early identification of potential high-risk populations for AIS, providing a new, quantifiable guidance scheme for the prevention and treatment of AIS in carotid atherosclerotic population.

Abstract:Renal artery stenosis (RAS) is a common disease that endangers human health, usually caused by atherosclerosis or fibromuscular dyspalsia. RAS is also one of the most common causes of secondary hypertension, often leading to resistant hypertension with markedly elevated renin levels and early onset of progressive renal insufficiency. In addition, the activation of renin-angiotensin-aldosterone system (RAAS) caused by RAS and pathophysiological changes including glomerular sclerosis and atrophy, water and sodium retention can also lead to cardiovascular events such as heart failure, pulmonary edema, coronary heart disease and cerebral infarction. Therefore, early recognition of RAS and prompt revascularization in patients with severe stenosis are key to the treatment of RAS. Percutaneous renal artery stenting (PRAS) has become the preferred revascularization for patients with RAS due to its high response rate, minimally invasiveness, fast recovery and low restenosis rate. However, there are still some unavoidable complications of PRAS, such as aortic dissection, renal artery rupture, puncture vascular aneurysm, contrast allergy and contrast-induced nephropathy. The occurrence of these complications may have adverse consequences for patients, and even death in severe cases. Renal arteriovenous fistula is a very rare complication of PRAS, and clinical experience in its recognition and management is very limited. Few cases that can be collected tend to favor re-surgical intervention. But surgical intervention undoubtedly increases the risk of patient suffering and mortality again. Thus, it is of great significance to summarize such complications and give a scientific recommendation to clinicians. This article reports a patient with resistant hypertension who underwent renal arteriography showing severe stenosis of renal vessels and developed a renal arteriovenous fistula after stent implantation. Therefore, it is worth considering whether the renal arteriovenous fistula caused by PRAS should be treated with surgical intervention or conservative medical treatment.

Abstract:Environmental factors such as air pollutants, plastic micro-particles, ionizing radiation, and traffic noise promote the onset and progression of atherosclerotic cardiovascular disease(CVD)through mechanisms including inducing inflammatory responses, promoting oxidative stress, and accelerating lipid deposition. Notably, the modification of apolipoprotein (Apo) by reactive oxygen species (ROS) accelerates this process. On one hand, ROS can oxidize key amino acid residues in Apo, altering its structure and thereby impairing its normal physiological function. On the other hand, ROS can induce lipid peroxidation of Apo, rendering the oxidized Apo more susceptible to recognition and uptake by macrophages. This accelerates foam cell formation and drives the progression of atherosclerotic (As) plaques. This review summarizes recent research advances on the role of ROS-induced modification of Apo by environmental factors in atherosclerotic CVD.

Abstract:Atherosclerosis is a chronic inflammatory disease and the root cause of most cardiovascular diseases. Soluble guanylate cyclase (sGC) agonists play an important role in the regulation of atherosclerotic diseases by nitric oxide (NO)/sGC/cyclic guanosine phosphate (cGMP) signaling pathway. sGC plays an anti-atherosclerotic role in reducing blood lipid levels, improving endothelial dysfunction, reducing inflammatory responses, inhibiting platelet activation, inhibiting smooth muscle cell proliferation and apoptosis via activating downstream cGMP. This article reviews the effect of sGC agonists on atherosclerosis and its mechanism, in order to provide a theoretical basis for the clinical application of sGC agonists.