Aim Acute aortic dissection (AAD) represents a cardiovascular ailment characterised by a notable mortality rate. Chronobiological patterns can offer a predictive framework for anticipating the onset of AAD. Method Data were gathered from 1,151 patients diagnosed with AAD at Changhai Hospital in Shanghai, China, spanning 2000-2023. The chi(2) test was used to assess whether specific periods exhibited significantly different seasonal/weekly distributions compared with others. Fourier models were utilised for the analysis of rhythmicity in monthly/circadian distribution. Publicly available genome-wide association studies datasets were used to establish the causal relationship between chronotype and AAD. Two sets of genetics instruments were used for analysis, derived from publicly available genetic summary data: 75 single-nucleotide polymorphisms (SNPs) significantly associated with chronotype; and SNPs associated with AAD in the FinnGen consortium. Results The mean age was 51.5 +/- 13.8 years, with 665 patients (57.8%) aged <55 years. Among the 1,151 patients, 80.9% were male. The distribution of DeBakey types was 73.2% (843) for DeBakey I, 21% (242) for DeBakey II, and 5.7% (66) for DeBakey III. Comorbidities included hypertension in 58.5% (673 cases) and diabetes in 7.8% (90 cases). A peak occurred during colder periods (winter/December), and a trough was noted in warmer periods (summer/June). Weekly distribution exhibited no significant variation. Fourier analysis revealed a statistically significant circadian variation (p<0.0001) with a trough between 23:00 and 00:00, a prominent peak from 07:00 to 08:00, and a minor peak between 20:00 and 21:00. Subgroup analyses identified circadian rhythmicity in all subgroups, except for the DeBakey III group and the female group. Using the 75 chronotype-related SNPs, evidence was found of a potential causal effect of chronotype on the risk of AAD, as the inverse-variance weighting analysis showed that self-report chronotype of morningness was associated with a decreased risk of AAD. Conclusions The findings substantiate that the initiation of AAD displays noteworthy seasonal, monthly, and circadian patterns. The Mendelian randomisation analysis also indicated that the onset of acute aortic dissection is related to circadian rhythm. These findings offer a fresh perspective, facilitating the identification of triggering factors for AAD and bolstering preventive measures for this catastrophic event.

Decellularized extracellular matrix (dECM), a promising tissue engineering scaffold for cardiovascular applications, might exhibit enhanced durability when endowed with anticalcification and antithrombotic properties. Herein, we present a biomimetic bilayer hydrogel coating applied to acellular swim bladders (ASBs). First, we designed an endothelium-mimicking (HCT) hydrogel coating, comprising alternately assembled endothelial glycocalyx macromolecule hyaluronic acid, copper ions, and tannic acid. Subsequently, a hydrophilic methacrylated silk fibroin (SilMA) hydrogel was incorporated as the outer coating layer. Notably, the HCT hydrogel penetrated and anchored into the ASB matrix, forming an interpenetrating network that enhanced the biostability and mechanical properties of the ASB matrix. Additionally, the SilMA hydrogel enhanced the hydrophilicity and antifouling properties of the HCT coating. In vitro experiments and subcutaneous implantation further revealed that the bilayer hydrogel (H/S) coating exhibited excellent biocompatibility, hemocompatibility, antibacterial activity, and anticalcification properties. Furthermore, a blood circulation model and rabbit shunt assay confirmed the great anticoagulation properties of the H/S coating. Moreover, in an in vivo rat carotid aorta replacement model, the H/S coating effectively promoted endothelialization, enhanced vascular remodeling, prevented calcification and thrombosis, and ultimately improved ASB durability. Based on these findings, our endothelium-mimicking hydrophilic bilayer hydrogel coating holds great promise as a surface modification strategy for tissue engineering scaffolds.

Background There is a paucity of data regarding surgical results of myocardial bridging(MB).Our study aimed to evaluate the clinical efficacy of surgical treatment including coronary artery bypass grafting (CABG) and unroofing for MB in symptomatic patients who had chest pain refractory to medical therapy.. Methods Among 124 adult patients diagnosed with myocardial bridging at our institution(2010–2019),85 underwent surgical intervention and 39 received medical treatment.To understand the potential benefit of surgical treatment,we excluded 21 patients with concomitant operations for other diagnoses or obstructive coronary disease.64 symptomatic patients with isolated left anterior descending(LAD) MB underwent surgical treatment,which included CABG for 56 patients and unroofing for 8 patients. All patients were followed up 1 to 10 years.We analyzed recurrent symptoms,postoperative medication use,and adverse cardiovascular events. Results Mean age was 60.9 ± 8.4 years(48 men [75%]).All patients underwent preoperative coronary angiography.Mean cardiopulmonary bypass and cross-clamp times were 53.5 ± 19.8 minutes and 24.0 ± 10.1 minutes,respectively.During follow-up(median, 28 months) there were no cardiac-related deaths.The reintervention rate after discharge in the operation group was lower than that in the non-operation group (14.3% vs. 35.9%, p = 0.027). The symptom improvement rate of patients in the operation group was higher than that in the non-operation group (82.8% vs 48.7%, p = 0.001). Through multivariate risk analysis, we found that antiplatelet strategies (p = 0.004, OR = 0.187, 95%CI = 0.059–0.594) were risk factors for graft restenosis in patients with CABG. Conclusions Surgical treatment can be performed safely and effectively in patients with chest pain and isolated LAD coronary artery myocardial bridging.However,patients should be aware of the potential for recurrent chest pain, and continued medical therapy was important.

Abstract Dilated cardiomyopathy (DCM), a major cause of heart failure in young adults, is characterized by ventricular dilation and progressive heart muscle dysfunction. Cellular mechanisms driving DCM have not been elucidated despite advances in genomic medicine. This study performed comprehensive multimodal single-cell analysis integrating RNA sequencing, assay for transposase-accessible chromatin with sequencing, and spatial transcriptomics data of cardiac tissues from patients with DCM and control subjects. The complex cellular heterogeneity and a novel neuro-cardiac interface were identified in DCM. The neuronal signaling pathways, including GABA receptor signaling and WT1 transcription factor activity, were profoundly dysregulated in the cardiomyocytes of patients with DCM. Cell-cell signaling analysis revealed that the communication patterns were altered, especially the upregulation of IGF and NRG signaling, suggesting a redefined role of adipocytes and lymphatic cells in DCM pathogenesis. The results of neuronal marker immunostaining analysis were consistent with those of bioinformatics analysis and indicated a potential cross-talk between cardiomyocytes and neurons. The findings of this study provided novel insights into the molecular mechanisms of DCM and identified potential therapeutic targets for DCM, which will enable the development of precision therapeutic approaches for cardiomyopathies.

Objective Calcific aortic valve disease (CAVD) is the leading cause of angina, heart failure, and death from aortic stenosis. However, the molecular mechanisms of its progression, especially the complex disease-related transcriptional regulatory mechanisms, remain to be further elucidated. Methods This study used porcine valvular interstitial cells (PVIC) as a model. We used osteogenic induced medium (OIM) to induce calcium deposition in PVICs to calcify them, followed by basic fibroblast growth factor (bFGF) treatment to inhibit calcium deposition. Transcriptome sequencing was used to study the mRNA expression profile of PVICs and its related transcriptional regulation. We used DaPars to further examine alternative polyadenylation (APA) between different treatment groups. Results We successfully induced calcium deposition of PVICs through OIM. Subsequently, mRNA-seq was used to identify differentially expressed mRNAs for three different treatments: control, OIM-induced and OIM-induced bFGF treatment. Global APA events were identified in the OIM and bFGF treatment groups by bioinformatics analysis. Finally, it was discovered and proven that catalase ( CAT ) is one of the potential targets of bFGF-induced APA regulation. Conclusion We described a global APA change in a calcium deposition model related to CAVD. We revealed that transcriptional regulation of the CAT gene may contribute to bFGF-induced calcium deposition inhibition.

Achondroplastic dwarfism is a rare hereditary metabolic disorder associated with a higher incidence of cardiovascular disease.There are few epidemiological data and surgical experience of rheumatic valvular disease in this population.This report is the only one to date on mitral replacement in an achondroplastic dwarfism.In addition, our approach involves placing the mechanical aortic valve prosthesis upside down in the mitral position.The 10-year results show benefits, but intraoperative management, valve type, and anticoagulation regimen are real challenges.

Abstract Objective Calcific aortic valve disease (CAVD) is a major cause of aortic stenosis resulting in angina, heart failure, and death. However, the molecular mechanism of its progression, especially the sophisticated disease-related transcriptional regulation machinery remains to be further elucidated. Methods This study was modeled on porcine valvular interstitial cells (PVIC). We used OIM to induce calcification and bFGF treatment to inhibit calcification. The mRNA expression profile of PVICs and their related transcriptional regulation were investigated using transcriptome sequencing. We used DaPars to further examine alternative polyadenylation (APA) among the different treatment groups. Results We identified global APA alteration in the OIM, OIM-bFGF, and Ctrl treatment groups. We also identified the CAT gene as one of the crucial candidate genes that may contribute to calcification inhibition through APA regulation. The alteration of both APA and protein levels of the CAT gene in the bFGF-treated group was further validated using qRT-PCR and western blotting analysis. Conclusion We described a global APA change in a calcification model related to CAVD. We revealed that transcriptional regulation of the CAT gene may contribute to bFGF-induced calcification inhibition.

Decellularization is a promising technique to produce natural scaffolds for tissue engineering applications. However, non-crosslinked natural scaffolds disfavor application in cardiovascular surgery due to poor biomechanics and rapid degradation. Herein, we proposed a green strategy to crosslink and functionalize acellular scaffolds via the self-assembly of copper@tea polyphenol nanoparticles (Cu@TP NPs), and the resultant nanocomposite acellular scaffolds were named as Cu@TP-dBPs. The crosslinking degree, biomechanics, denaturation temperature and resistance to enzymatic degradation of Cu@TP-dBPs were comparable to those of glutaraldehyde crosslinked decellularized bovine pericardias (Glut-dBPs). Furthermore, Cu@TP-dBPs were biocompatible and had abilities to inhibit bacterial growth and promote the formation of capillary-like networks. Subcutaneous implantation models demonstrated that Cu@TP-dBPs were free of calcification and allowed for host cell infiltration at Day 21. Cardiac patch graft models confirmed that Cu@TP-dBP patches showed improved ingrowth of functional blood vessels and remodeling of extracellular matrix at Day 60. These results suggested that Cu@TP-dBPs not only had comparable biomechanics and biostability to Glut-dBPs, but also had several advantages over Glut-dBPs in terms of anticalcification, remodeling and integration capabilities. Particularly, they were functional patches possessing antibacterial and proangiogenic activities. These material properties and biological functions made Cu@TP-dBPs a promising functional acellular patch for cardiovascular applications.

Background Dual antiplatelet therapy (DAPT) improves early post-operative graft patency, but the optimal DAPT strategy for the patients after coronary artery bypass grafting (CABG) has not been confirmed. We sought to evaluate the effect of aspirin plus ticagrelor versus aspirin plus clopidogrel on saphenous vein graft (SVG) patency within 1 year after CABG. Methods Between October 2017 and December 2018, 147 consecutive patients undergoing elective CABG at Changhai Hospital were randomized into two groups: group AT, receiving aspirin 100 mg/d plus ticagrelor 2×90 mg/d; group AC, receiving aspirin 100 mg/d plus clopidogrel 75 mg/d. Both DAPTs should be administered within 24 h when clinical stability was ensured. 64-multislice computed tomography angiography (MSCTA) was used to assess the graft patency at 12 months after CABG.CYP2C19 gene variants were measured to assess the clopidogrel efficacy on graft patency. Results Among the 147 participants who completed the study, one (0.7%) patient from the AC group died at 5 weeks after surgery due to severe infection. All other patients were treated with DAPT for 12 months and underwent 64-MSCTA according to schedule. There were no significant differences in pre-operative characteristics and intraoperative transit-time flow measurement findings between the two groups. Besides, no significant differences in the incidence of major adverse cardiac events (MACEs) and major bleeding were observed. A 64-MSCTA showed that SVG patency was 91.0% (141 of 155) in the AT group and 89.9% (161 of 179) in the AC group (P=0.751). No significant associations were found between different CYP2C19 genotypes and SVG patency (P>0.05). Conclusions Either aspirin plus ticagrelor or aspirin plus clopidogrel can maintain a fairly high graft patency rate in the early phase after CABG, regardless of CYP2C19 genotypes.

Objective:To summarize the results and methods of surgical treatment for type A aortic dissection with small true lumen of the descending aorta.Methods:9 patients underwent surgical treatment for type A aortic dissection with small true lumen of the descending aorta between January 2017 and December 2019 were analyzed retrospectively. There were 7 males and 2 females, mean age of (41.6±9.2) years. Acute dissection were 2 cases, and chronic dissection were 7 cases. Preoerative computed tomography was used to diagnose the dissection and evaluate the true lumen of the descending aorta. This procedure was done in all patients via a median sternotomy under hypothermic CPB with SCP. 4-branched prosthetic graft was used to replace the ascending aorta and aortic arch. The procedures involving the descending aorta: Hybrid surgery using TEVAR. Distal intimal flap fenestration. Implanting the intraoperative stent-graft or prosthetic graft at false lumen for second-step operation.Results:There was no in-hospital mortality. Stroke, Spinal cord, visceral ischemia and lower limbs malfunction were not observed. Reintervention was not found in case with acute dissection during follow-up. One patient who reveived fenestration underwent TEVAR, others with chronic dissection underwent thoracoabdominal aortic replacement 3 months after surgery.Conclusion:Hybrid or staged procedures was a suitable alternative to patients with type A aortic dissection with small true lumen of the descending aorta.

目的 分析心脏移植患者术后早期三尖瓣反流的风险因素,总结心脏移植供受体评估及心脏移植围手术期的管理经验,以期提高心脏移植术后患者生存率、降低移植术后患者早期右心功能不全发生率.方法 选取2017年3月至2019年11月在我院接受同种原位心脏移植手术的74例患者作为研究对象,按术后三尖瓣反流束面积与右心房面积比值将患者分为两组:组1(15例,三尖瓣反流束面积与右心房面积比值<20％)和组2(59例,三尖瓣反流束面积与右心房面积比值≥20％).根据供体心脏标准获取心脏,术前通过Swan-Ganz导管监测患者肺动脉收缩压(PAPs)等指标,采用超声心动图评价患者术后30 d内的三尖瓣反流程度.采用多因素logistic回归模型分析移植术后三尖瓣反流的影响因素.结果 原发性移植物功能衰竭(PGF)、急性排斥反应、供受体体重比和术前PAPs在两组间的差异均有统计学意义(P均<0.01),两组供体年龄、受体年龄、供受体性别是否匹配、术前NYHA心功能分级、原发病种类、供受体身高比、术前总胆红素水平及术前右心室前后径等的差异均无统计学意义(P均>0.05).多因素logistic回归分析结果显示PGF(OR=1.892,95％CI 1.150～1.972)、急性排斥反应(OR=1.625,95％CI 1.190～1.885)、供受体体重比(OR=0.001,95％CI 0.000～0.873)和术前PAPs(OR=1.274,95％CI 1.099～1.498)是患者心脏移植术后早期三尖瓣反流的影响因素(P均<0.05).结论 注重供受体体重的匹配、防治围手术期肺动脉高压、严格应用免疫抑制剂及预防PGF有利于降低心脏移植术后早期三尖瓣反流,减少右心功能衰竭发生.

目的 本研究总结及分析近十年接受首次外科干预时年龄已超过6个月龄室间隔完整型肺动脉闭锁(PA/IVS)患者的外科治疗策略.方法 回顾2007年1月至2018年12月,上海儿童医学中心共收治63例年龄超过6个月的PA/IVS患者,其首次干预时的年龄为6.2～79.6(20.1)个月,体重为4.6～17.5(9.5)kg,将其中51例已获终期治疗的患者分为3组,包括双心室组11例、一个半心室组18例和单心室组22例,并对各组右室发育程度、术后生存率、再次手术干预率及中远期心功能状况进行比较分析.结果 术后随访时间为0.6～11.9(5.5)年,失访5例,死亡3例(5.9％,3/51).其中,双心室组右室发育不良均为轻或中度(中度占45.5％),一个半心室组以中度为主(中度占94.4％),单心室组则为重度为主(中度占13.6％),各组三尖瓣Z值比较具有统计学差异(P<0.01).双心室组、一个半心室组和单心室组大多数患者中远期随访结果良好,各组术后十年免再手术干预率分别为75.8％、85.2％和76.8％(P>0.05),心功能分级大多数患者均为Ⅰ或Ⅱ级,仅一个半心室1例和单心室组2例为Ⅲ级.结论 大年龄PA/IVS患者由于右心室生长潜能受到限制而导致较大比例患者失去双心室矫治机会,但依据右室发育不良程度选择个性化的手术方案,最终都可获得较低死亡率,且中远期生存质量良好.

目的 探讨经胸微创介入术治疗小儿先天性心脏病复合畸形的临床效果.方法 回顾性分析60例先天性心脏病复合畸形患儿的临床资料,根据治疗方法不同将患儿分为对照组与试验组,各30例.对照组采用常规开胸手术治疗,试验组采用经胸微创介入手术治疗.比较两组患者的临床治疗效果.结果 术后6个月,试验组的LVSV高于对照组,LVEF低于对照组(P<0.05).试验组的手术时间、术后住院时间均短于对照组,手术成功率高于对照组,术后并发症总发生率低于对照组(P<0.05).结论 经胸微创介入术治疗小儿先天性心脏病复合畸形的效果显著,可改善患儿的心功能,提高手术成功率,降低术后并发症发生率.

Background To analyze the risk factors of chronic left ventricular dysfunction (LVD) after cardiac valve surgery. Methods A retrospective analysis of 860 patients who underwent heart valve surgery in our center from January 2017 to December 2018, including 650 males and 210 females, aged 58±5.8 years. Inclusion criteria: (I) the patient was clinically diagnosed with heart valve disease and met the surgical indications for mitral valve replacement (MVR), mitral valve repair (MVP), aortic valve replacement (AVR) and double valve replacement (DVR); (II) if atrial fibrillation, coronary artery disease, and tricuspid regurgitation are combined before surgery, radiofrequency ablation, coronary bypass and tricuspid angioplasty were performed contemporarily. Exclusion criteria: (I) preoperative LVEF <50%; (II) aortic dissection underwent Bentall and right heart valve replacement procedures; (III) cardiopulmonary resuscitation and death during perioperative period and 6 months after operation; (IV) postoperative CRRT, IABP, or ECMO assistance; (V) postoperative cardiac dysfunction due to valvular dysfunction, perivalvular leak, or infective endocarditis. Patients were divided into LVD group (LVEF <40%) and control group (LVEF ≥40%) based on cardiac LVEF at 6 months after surgery. Logistic regression was used to analyze the risk factors of postoperative LVD. Results There were 126 cases in LVD group and 734 cases in control group. There were significant differences in preoperative coronary artery disease, atrial fibrillation, pulmonary hypertension, NYHA classification, left ventricular end diastolic diameter (LVEDD), and left ventricular end systolic diameter (LVESD) between the two groups (P<0.05). The differences in the changes of LVEDD and LVESD before and after operation between the two groups were statistically significant (P<0.05). Logistic regression analysis showed that preoperative LVEDD >55 mm, preoperative LVESD >40 mm, preoperative combined atrial fibrillation, preoperative combined pulmonary hypertension, preoperative NYHA III–IV, and preoperative combined coronary artery disease were the risks of postoperative chronic LVD. Conclusions The left ventricular diameter, preoperative coronary artery disease, NYHA III–IV, preoperative atrial fibrillation, and preoperative pulmonary hypertension are risk factors for chronic LVD after heart valve surgery.

Objective:To explore the treatment strategy and prognosis of primary graft dysfunction(PGD)after heart transplantation.Methods:A retrospective review was performed for 74 consecutive patients undergoing orthotopic heart transplantation between March 2017 and September 2019. Basiliximab was prescribed as an immune induction therapy. Over that time period, 14 patients developed PGD and required extracorporeal membrane oxygenation(ECMO)and/or intra aortic balloon pump(IABP)support. They were 13 males and 1 female with a mean age of (51.1±9.5)(30~63)years. Donor age was(42.7±6.5)(29~53)years, weight ratio of donor/recipient(0.91±0.12)(0.73~1.27)and ischemic time(251.2±117.5)(62~370). Diagnosed by interoperative transesophageal echocardiography, PGD was defined as having a need for supporting of ECMO and/or IABP during immediate post-operation because of impossibility of weaning from cardiopulmonary bypass. The specific procedures included ECMO(2 cases), ECMO+ IABP(8 cases)and IABP(4 cases).Results:The incidence of PGD was 18.9%(14/74). And 80% patients were successfully weaned from ECMO, 100% stayed off from IABP and 5 patients died in-hospital. Duration of ECMO support was (154.2±46.5)(104~216)hours and IABP support time (176.2±64.5)(78~288)hours. The survivors were followed up for 1~24 months, Ultrasound cardiogram ohowed that cardiac contractile function was satisfied. There was no instance of transplant rejection or cardiovascular adverse event.Conclusions:As a life-threatening condition, PGD is a leading cause of early death after heart transplantation. ECMO and/or IABP support for PGD patients after heart transplantation may yield a satisfactory long-term prognosis.

This study aimed to report the case of 7 consecutive patients who underwent surgical treatment for aortic endograft infection after thoracic endovascular aortic repair (TEVAR). The management included the reconstruction of aorta using extra-anatomic prosthetic graft bypass (between the ascending aorta and the abdominal aorta), removal of the infected endograft with debridement of the infected tissue and sac drainage, followed by prolonged antibiotic therapy. This brief communication highlights that the reconstruction of aorta using extra-anatomic prosthetic graft bypass during surgical treatment for aortic endograft infection after TEVAR was reliable and effective.

Background: Surgical strategy for treating chronic type A dissection with small true lumen at the descending aorta has not been reported. In this retrospective study, we reviewed our experience of applying a two-stage procedure for treating chronic type A dissection with small true lumen at the descending aorta. Methods: Between February 2016 and December 2019, seven patients suffering from chronic type A dissection with small true lumen at the descending aorta underwent this procedure. Preoperative computed tomographic angiography (CTA) was performed to carefully assess the diameter of the descending aorta, tear site, and visceral arteries. The interval between the two procedures is determined by the condition of the patients' recovery and illustration of postoperative CTA after the first stage procedure. Results: All patients underwent first- and second-stage procedures. No mortality was observed among the seven patients. One patient who had a transient neurological deficit after the first stage recovered completely before hospital discharge. In two patients, the diameter of the descending aorta was enlarged postoperatively after the first-stage procedure. The interval between the two procedures was 2- 3 months. However, no adverse events, such as stroke, paraparesis, visceral malperfusion, and lower extremity malfunction, were observed. Conclusions: The two-staged procedure for the repair of chronic type A dissection with small true lumen at the descending aorta is adaptable with low prevalence of mortality and complication.

目的 研究大动脉转位(TGA)患儿行一期大动脉调转术(ASO)后应用大剂量血管活性药物的有效性及安全性.方法 选取2009年1月至2019年1月在中国人民解放军南部战区总医院心脏外科行ASO并术后使用血管活性药物的82例TGA患儿为研究对象,根据术后血管活性药物(肾上腺素和去甲肾上腺素)的使用剂量将其分为A组[20例,0.01～0.10μg/(kg·min)]、B组[32例,0.11～0.20μg/(kg·min)]及C组[30例,0.21～0.40μg/(kg·min)].比较三组患儿的并发症发生情况、用药时间、手术时间、术后住院时间、体外循环时间及应用血管活性药后的不良反应发生情况.结果 A、B、C组患儿早期死亡率分别为15.0％(3/20)、15.6％(5/32)、10.0％(3/30),差异无统计学意义(P>0.05).三组患儿并发症总发生率、用药时间和手术时间比较,差异具有统计学意义(P<0.05),其中,C组的并发症总发生率最低.A、B、C组使用血管活性药物后分别有13、8、5例发生不良反应,三组低心排征、乳酸>4.0 mmol/L的发生率比较,差异具有统计学意义(P<0.05).结论 TGA患儿ASO术后早期死亡率仍较高;为维持患儿生命体征平稳,大剂量使用血管活性药物是安全、有效的,且未增加患儿的早期死亡率和术后并发症发生率.

Phenotypic switch of vascular smooth muscle cells (VSMCs) plays an important role in the pathogenesis of atherosclerosis and aortic dissection. However, the mechanisms of phenotypic modulation are still unclear. MicroRNAs have emerged as important regulators of VSMC function. We recently found that microRNA-124 (miR-124) was downregulated in proliferative vascular diseases that were characterized by a VSMC phenotypic switch. Therefore, we speculated that the aberrant expression of miR-124 might play a critical role in human aortic VSMC phenotypic switch. Using quantitative RT-PCR, we found that miR-124 was dramatically downregulated in the aortic media of clinical specimens of the dissected aorta and correlated with molecular markers of the contractile VSMC phenotype. Overexpression of miR-124 by mimicking transfection significantly attenuated platelet-derived growth factor-BB-induced human aortic VSMC proliferation and phenotypic switch. Furthermore, we identified specificity protein 1 (Sp1) as the downstream target of miR-124. A luciferase reporter assay was used to confirm direct miR-124 targeting of the 3'-untranslated region of the Sp1 gene and repression of Sp1 expression in human aortic VSMCs. Furthermore, constitutively active Sp1 in miR-124-overexpressing VSMCs reversed the antiproliferative effects of miR-124. These results demonstrated a novel mechanism of miR-124 modulation of VSMC phenotypic switch by targeting Sp1 expression.NEW & NOTEWORTHY Previous studies have demonstrated that miR-124 is involved in the proliferation of a variety of cell types. However, miRNAs are expressed in a tissue-specific manner. We first identified miR-124 as a critical regulator in human aortic vascular smooth muscle cell differentiation, proliferation, and phenotype switch by targeting the 3'-untranslated region of specificity protein 1.

Cancer stem cells (CSCs) represent a subpopulation of tumor cells that exhibit capacities for tumor initiation and progression. Identifying CSCs and their related pathways is necessary for the development of new therapeutic targets against tumors. However, the molecular mechanism of CSCs in esophageal squamous cell carcinoma (ESCC) remains elusive. This study demonstrated that OV6 expression was closely associated with ESCC patients' clinical outcome and prognosis. OV6+ cells possessed stronger stem-like properties, including self-renewal, stem cell-associated gene expression, tumorigenicity, chemo-resistance, invasion, and metastasis. Autophagy maintained the stem-like properties of OV6+ cells by stabilizing ATG7-dependent β-catenin. Furthermore, a significantly positive correlation between ATG7 and OV6 expression was detected in human ESCC biopsies, and this correlation could be used to predict ESCC patients' prognosis. Taken together, our findings provide a novel potential CSC marker for ESCC. OV6+ cancer stem cells can promote the progression of ESCC through ATG7-dependent β-catenin stabilization. OV6 may serve as a novel prognostic biomarker and therapeutic target for ESCC patients.