Doxorubicin (DOX) is a widely used and efficacious anthracycline in clinical practice for the treatment of various tumors; however, a major limitation of DOX therapy is its cardiotoxicity, which significantly restricts its clinical application. Mitochondria in the heart are particularly susceptible to the deleterious effects of DOX, resulting in mitochondrial dysfunction, reactive oxygen species generation, cardiomyocyte apoptosis, bioenergetic failure, and impaired cardiac function. Mitochondrial sirtuins (SIRT3 and SIRT4) play pivotal roles in these cellular processes. Sirtuin-3 (SIRT3), a member of the mitochondrial Sirtuin family, effectively attenuates DOX-induced myocardial injury by suppressing inflammation and oxidative damage while improving mitochondrial function. Therefore, SIRT3 is a key regulator involved in multiple mechanisms underlying DOX-induced cardiotoxicity. Several studies have shown the protective effects of SIRT3 against DOX-induced myocardial injury and have provided insights into its potential for future clinical applications.

Growth differentiation factor-15 (GDF-15), a member of the TGF-beta superfamily, is upregulated in response to tissue ischemia and proinflammatory cytokines that promote the onset and progression of atherosclerosis. Given that GDF-15 is also elevated in individuals with kidney dysfunction compared to those without, GDF-15 levels may contribute to pathways that play a role in chronic kidney disease-associated atherosclerosis.

In 338 patients with coronary artery disease, we investigated the association between GDF-15 and plaque morphology assessed by intravascular ultrasound. No association was found between log-transformed GDF-15 levels and the percentage of calcified plaque volume in chronic kidney disease (CKD) stages G1-G2 (r = 0.077, P = 0.328) or G3a (r = 0.012, P = 0.910). In contrast, a significant association was observed in stages G3b-G5 (r = 0.275, P < 0.001).

Multiple linear regression analysis showed that the highest GDF-15 tertile (≥ 2,567 ng/L) as a categorical variable and GDF-15 levels were associated with the calcified plaque percentage in the CKD stages G3b-G5 (n = 82, Estimate [95% confidence interval], 0.0038 [0.0004, 0.0071]; P = 0.0027). This association was also observed with GDF-15 as a continuous variable (estimate per 2-fold higher, 0.0128 [0.0028, 0.2281]; P = 0.0013). No association was found for other CKD stages.

A significant association was found between elevated GDF-15 levels and the presence of calcified coronary plaques, as assessed by intravascular ultrasound, in patients with coronary artery disease and CKD.

Heart failure is associated with poor outcomes in ST-elevation myocardial infarction (STEMI). While heart failure following STEMI has been extensively studied, the role of a prior history of heart failure hospitalization (HFH) as a specific risk factor for long-term outcomes in patients with STEMI who underwent primary percutaneous coronary intervention (PCI) has not been fully explored.

Consecutive 1,544 patients (median age, 69 [60-78] years; male, 75.1%) who presented to the hospital within 24-hours after symptom onset and underwent primary PCI were evaluated. The predictive risk factors for long-term cardiac mortality were analyzed using the random survival forest method. In addition, a Cox proportional hazards regression analysis was performed to assess the independent impact of HFH on cardiac mortality.

Among the cohort, 26 patients (1.7%) had a HFH. During a median follow-up of 5.6-years, 173 (11.2%) patients died due to cardiac disease. In the Kaplan-Meyer analysis, patients with HFH showed a significantly higher cardiac mortality than those without HFH (log-rank, P < 0.001). In order of importance, estimated glomerular filtration rate, the necessity of intubation, age, Killip class, left ventricular ejection fraction, HFH, serum albumin, and serum brain natriuretic peptide were identified as predictive risk factors of cardiac mortality. The multivariate Cox regression model revealed that HFH was a significant independent risk predictor of cardiac mortality (hazard ratio: 3.587; 95% confidence interval: 1.687-7.624; P < 0.001).

HFH may independently increase the long-term risk of cardiac mortality by 4-fold in patients with STEMI undergoing primary PCI.

Atrial fibrillation (AF) is a common arrhythmia that can reduce the quality of life of patients. Observational studies have reported that work and sleep are associated with the development of AF, but the causal relationship is unclear.

Based on published genome-wide association studies (GWASs), we conducted a two-sample Mendelian Randomization (MR) analysis employing inverse variance weighted (IVW), weighted median, and MR-Egger regression analyses. We chose statistical data of 3 work factors from the MRC-IEU GWAS pipeline and 2 sleep factors from the Sleep Disorders Knowledge Portal as the exposure and the FinnGen study of AF as the outcome.

The study revealed that engaging in heavy physical work was associated with an increased risk of AF (IVW OR, 1.787; 95% CI, 1.082-2.853; P = 0.023), and job satisfaction was negatively correlated with AF risk (IVW OR, 0.719; 95% CI, 0.536-0.964; P = 0.028). In addition, jobs that primarily involved walking or standing, short sleep duration (< 7 hours), and long sleep duration (≥ 9 hours) were not associated with AF. The results of the sensitivity analysis are consistent with these trends.

The results support a causal relationship between heavy physical labor and increased risk of AF, and that job satisfaction has some protective effect on AF.

Catheter ablation for atrial fibrillation (AF) is now a commonly performed procedure with improved techniques. Several studies have evaluated sex differences in AF, including efficacy and safety of catheter ablation, with inconsistent findings.

We compared the characteristics, success rate, and complications of catheter ablation in patients with AF focusing on sex differences. A total of 368 consecutive AF patients (men 254, women 114) who underwent catheter ablation from January 2017 to March 2022 at our institution were analyzed. Effects of catheter ablation on cardiac function in the left ventricle (LV) and left atrium (LA), and plasma B-type natriuretic peptide levels were evaluated at baseline and at 1-year follow-up.

Women underwent catheter ablation at an older age and with a lower body mass index (BMI) than men, but the recurrence rate at 1 year showed no significant difference. Among patients with paroxysmal AF (PAF), procedural complications occurred more often in women than in men after radiofrequency catheter ablation, but not after cryoballoon ablation. At 1 year after ablation, the LV ejection fraction, LA volume index, and LA emptying fraction were improved in women as well as in men, particularly in non-PAF patients.

Our findings indicate that catheter ablation for AF is effective in women, similar to men, particularly in terms of LA structure and function, despite being performed at an older age and in non-PAF patients. Additionally, cryoballoon ablation may be a suitable alternative to radiofrequency ablation in women with PAF.

This study aimed to explore the clinical value of galectin-3 (Gal-3) and heart-type fatty acid-binding protein (H-FABP) levels in the diagnosis and prognosis of viral myocarditis (VMC) in children.

A case group and a control group were established. The distribution of infected viruses in the case group was analyzed, and serum Gal-3 and H-FABP levels were compared between the case and control groups, and among different disease severity and prognostic subgroups within the case group.

A total of 114 viral strains were isolated from 110 children, with coxsackievirus B being the most prevalent. The case group showed higher serum Gal-3 and H-FABP levels than the control group. Within the case group, the moderate and severe subgroup showed higher serum Gal-3 and H-FABP levels than the mild subgroup, and children with poor prognosis showed significantly elevated levels compared with those with good prognosis. Receiver operating characteristic curve analysis showed that the AUC (95% CI) for pediatric VMC diagnosis using serum Gal-3, H-FABP, and their combination were 0.844, 0.800, and 0.890, respectively. For predicting poor prognosis in VMC, the AUC values for Gal-3, H-FABP, and their combination were 0.823, 0.809, and 0.885, respectively.

Serum Gal-3 and H-FABP levels are significantly elevated in children with VMC. Their combined measurement offers enhanced diagnostic and prognostic value, aiding in the early identification and risk assessment of VMC in pediatric patients.

Wild-type transthyretin cardiac amyloidosis (ATTRwt-CA) is a life-threatening condition caused by the deposition of amyloid fibrils from misfolded transthyretin in the myocardium. While protein misfolding underlies its pathogenesis, the triggers and factors driving disease progression remain unclear. This study explores the relationship between lifestyle factors, particularly oxidative stress, and the incidence of ATTRwt-CA. A lifestyle questionnaire survey was conducted among patients with and without ATTRwt-CA at Kochi Medical School Hospital, Japan. Multivariate regression models were used to assess the odds of ATTRwt-CA occurrence in individuals with identified risk factors. The mean ages of patients in the ATTRwt-CA group (n = 65) and the non-ATTRwt-CA group (n = 65) were 77.9 ± 6.5 years and 78.5 ± 7.4 years, respectively. Multiple logistic regression analysis identified male sex (adjusted odds ratio, 4.35; 95% confidence interval, 1.39-14.29; P = 0.01) as an independent risk factor for ATTRwt-CA. Past sunlight exposure of ≥ 1 hour per day (adjusted odds ratio, 3.21; 95% confidence interval, 0.87-11.88; P = 0.08) showed a tendency towards a positive association with ATTRwt-CA occurrence. In contrast, past black tea consumption (adjusted odds ratio, 0.13; 95% confidence interval, 0.01-1.28; P = 0.08) and past smoking (adjusted odds ratio, 0.29; 95% confidence interval, 0.12-0.72; P < 0.01) were tentatively or significantly associated with ATTRwt-CA occurrence. Lifestyle factors may be linked to the occurrence of ATTRwt-CA, potentially through mechanisms involving oxidative stress.

Despite advancements in heart failure (HF) therapies, managing symptoms and congestion remains challenging for some patients. Adaptive servo-ventilation (ASV) has been used in Japan to treat residual congestion in chronic HF, but its efficacy remains debated.

This study is a subanalysis of the SAVIOR-L study, a multicenter prospective observational study in Japan evaluating ASV in worsening HF. The study included 96 ASV users (ASV group) and 288 non-ASV users (non-ASV group) selected via propensity score matching. The primary outcome was a hierarchical composite of cardiovascular death and cardiovascular-related hospitalization, assessed using a win ratio analysis.

The win ratio (95% CI) for ASV was 0.838 (0.657-1.069) in the matched-pair method and 0.850 (0.829-0.872) in the unmatched-pair method. Furthermore, the results of the win ratio analysis using the matched-pair method remained consistently neutral even in stratified analyses based on heart failure severity.

The results indicate that ASV use in worsening HF has a neutral effect on prognosis. While ASV does not appear to be definitively harmful, its benefits remain uncertain. Therefore, its use requires careful consideration in clinical practice.

Maternal hypertensive disorder (MHD) is one of the leading causes of maternal and perinatal mortality. With the adjustment of China's population policy and social development, identifying and monitoring the changing trends in the burden of MHD is significant for disease prevention and control.

This research aimed to determine the temporal trends of the MHD burden in China from 1990 to 2021.

Using data from the GBD Study 2021, this research analyzed trends in the incidence, morbidity, mortality, and disability-adjusted life years (DALYs) as well as age-standardized rates (ASRs) of MHD in China from 1990 to 2021. Joinpoint regression analysis was executed to evaluate temporal trends and their key turning points, with the age distribution of disease burden between 1990 and 2021 compared. Temporal trends in the burden of maternal hypertension due to iron deficiency were also analyzed.

In 2021, there were 691,387 new cases of maternal hypertension in China, with 151,917 cases suffering from the disease, 173 deaths, and a loss of 17,530 in DALYs, representing decreases of 44.629%, 43.695%, 89.658%, and 84.970%, respectively, compared to 1990. Death and DALY indicators continued to decline, while incidence and prevalence indicators showed an "inverted N-shaped" fluctuation. Joinpoint regression analysis demonstrated that between 1990 and 2021, age-standardized incidence rate, prevalence rate, mortality rate, and DALY rate all significantly declined, with average annual percentage changes of -1.398 (95% CI: -1.738, -1.056), -1.360 (95% CI: -1.704, -1.014), -6.770 (95% CI: -7.272, -6.264) and -5.551 (95% CI: -5.908, -5.193), respectively. The age distribution of disease burden shifted greatly, with the main burden population shifting from ages 20-24 in 1990 to ages 30-34 years in 2021. During the same period, deaths and DALYs, as well as their corresponding ASRs induced by iron deficiency-related MHD, exhibited continuing downward trends.

The overall disease burden of MHD in China is on a declining trend, but the main burden is shifting toward older age groups. In the future, efforts should focus on strengthening stratified management for older pregnant women and further investigating factors influencing the disease burden to optimize prevention strategies and implement targeted interventions.

Cardiometabolic multimorbidity (CMM) is the co-occurrence of 2 or more cardiometabolic diseases, such as cardiovascular disease, stroke, diabetes, and hypertension. This study explores how leisure activities influence the risk of CMM in older Chinese adults using a prospective cohort database.

The study analyzed 9,988 participants aged 65 and older from the Chinese Longitudinal Healthy Longevity Survey (CLHLS), assessing CMM risk as the outcome. A Cox proportional hazards regression model was used to assess the impacts of individual leisure activities on CMM risk, while a Restricted cubic spline (RCS) Cox regression model explored the dose-response relationship between activity diversity and CMM. Stratified analyses by age, gender, BMI, and residence were also conducted, and a sensitivity analysis was performed for robustness.

Frequent housework (HR: 0.79, 95% CI: 0.70-0.89) and pet/livestock ownership (HR: 0.70, 95% CI: 0.61-0.80) lowered CMM risk by 21% and 30%, respectively. However, frequent TV/radio viewing (HR: 1.17, 95% CI: 1.03-1.34) raised CMM risk by 17%. There was no significant association between the activity diversity score and the risk of co-morbidities among the elderly (P for overall > 0.05), but activity diversity was associated with the risk of co-morbidities among the lower-aged (< 85 years) elderly group after age stratification (P for overall = 0.05). Activity diversity was also associated with the risk of co-morbidities in the rural elderly group (P for overall = 0.05).

Regular housework and pet/livestock ownership reduced CMM risk in older adults, while TV/radio viewing increased it. The influence of leisure activities on CMM risk varied by age, gender, BMI and residence.

The aim of this study was to investigate the mechanism of m6A methylation in pathological myocardial hypertrophy (PMH), focusing on whether the methyltransferase METTL3 regulates the expression and nuclear translocation of the transcription factor EB (TFEB), thereby affecting autophagic activity and exacerbating the development of myocardial hypertrophy.

An in vivo PMH model was established in mice via transverse aortic constriction (TAC), and an in vitro hypertrophy model was established using H9C2 cells stimulated with angiotensin II (AngII). HE staining, Western blotting, qRT-PCR, immunofluorescence, and dual-color autophagy flux analyses were employed to detect the expression of autophagy-related proteins (LC3, Beclin-1, P62, ATG5) and apoptosis levels. Changes in TFEB and key m6A-related enzymes (METTL3, ALKBH5, heterogeneous nuclear ribonucleoprotein D [HNRNPD]) were examined, and gene overexpression or knockdown experiments were performed to clarify their roles in regulating autophagy and myocardial hypertrophy. Finally, m6A MeRIP-qPCR and RIP-qPCR were conducted to explore the effect of METTL3 on m6A modification and the stability of TFEB transcripts, verifying the interplay between METTL3 and TFEB and its impact on autophagy.

In both the in vivo and in vitro hypertrophy models, autophagy was significantly impaired and apoptosis was elevated, while TFEB mRNA and protein expression and its nuclear localization were clearly reduced. At the same time, global m6A methylation was markedly increased, accompanied by upregulation of METTL3 and HNRNPD, as well as downregulation of ALKBH5. Functional assays indicated that METTL3 overexpression further inhibited autophagy-related protein expression and autophagic flux, whereas METTL3 knockdown partially restored autophagy. Mechanistic studies revealed that METTL3 modulates TFEB pre-mRNA stability by influencing the binding efficiencies of ALKBH5 and HNRNPD, resulting in decreased TFEB expression. Conversely, overexpression of TFEB could partly counteract the autophagy impairment caused by METTL3 overexpression and reciprocally regulate the expression of METTL3, ALKBH5, and HNRNPD.

METTL3 mediates the inhibition of TFEB via m6A modification, thereby impairing autophagy and aggravating myocardial hypertrophy. These findings suggest that the m6A-TFEB axis may serve as a novel therapeutic target for preventing and treating myocardial hypertrophy and heart failure, offering new insights into the intervention of cardiac remodeling-related diseases.

Evidence suggests that autophagy plays a crucial role in myocardial ischemia/reperfusion (I/R) injury. Renalase (RNLS) plays a protective role in cardiovascular diseases, including myocardial ischemia/reperfusion injury (MI/RI). Therefore, we used both in vivo and in vitro I/R models to monitor autophagy in the cardiomyocytes by exposing H9c2 cells to oxygen and glucose deprivation/reoxygenation (OGD/R) and subjecting rats to I/R, respectively. Wistar rats (male, 8 weeks, n = 27) were randomly divided into a Sham group, I/R + Vehicle group, and I/R + recombinant renalase protein (Re-RNLS) group. An MI/RI model was induced by left anterior descending artery ligation/release, TTC-Evans blue double staining was utilized to evaluate the area of myocardial infarction and ischemic area 24 hours after the operation, and plasma lactate dehydrogenase (LDH) and creatine kinase (CK) activities, plasma RNLS, epinephrine, and dopamine concentrations were detected by ELISA. H9c2 cells were treated with OGD/R serum and pretreated with Re-RNLS, chloroquine (CQ), and MK2206. Western blotting detected protein expression changes in LC3 autophagosomes were monitored by immunofluorescence, and cell death was determined by flow cytometry. The level of RNLS in serum was significantly increased during MI/RI in rats, and Re-RNLS significantly reduced myocardial infarct size after I/R surgery (24.6 ± 4.1% versus 11.2 ± 1.2%). RNLS deficiency aggravated the OGD/R injury in H9c2 cells, and Re-RNLS inhibited the expression of LC3 and Beclin-1 in H9c2 cells subjected to OGD/R, thereby reducing autophagosome formation. Re-RNLS activated the Akt/mTOR pathway of H9c2 cells to play a cytoprotective role. RNLS protects against MI/RI injury by inhibiting autophagy through activating the Akt/mTOR pathway.

The incidence of acute myocardial infarction (AMI) is increasing, and existing diagnostic techniques exhibit limited capacity for early AMI diagnosis. Given the robust association between Ca²⁺ levels and the AMI initiation, calcium-related genes represent promising biomarkers for the early diagnosis of AMI.

The expression data of patients with AMI and normal samples were obtained from the gene expression omnibus database. Weighted correlation network analysis (WGCNA) was applied to identify genes associated with AMI. Signature genes were screened using the least absolute shrinkage and selection operator, support vector machine-recursive feature elimination (SVM-RFE), and random forest algorithm. A diagnostic model based on the signature gene was established and evaluated. The CIBERSORT algorithm was used to determine the levels of immune cell infiltration, and the single-sample gene set enrichment analysis (ssGSEA) scores of the immune cells were calculated. The regulatory network of competing endogenous RNA (ceRNA) based on the signature genes was constructed using cytoscape. The DGIdb database was used to identify potential drugs for AMI that may interact with the signature genes.

A high-performance diagnostic model based on four signature genes was established. The CIBERSORT algorithm and ssGSEA analysis revealed differences in immune cells between the patients with AMI and normal groups. The ceRNA regulatory network revealed multiple lncRNA and miRNA targeting signature genes. Niacin, nitroglycerin, arsenic disulfide, and quercetin are potential drugs that interact with the signature genes.

Four signature genes were selected as calcium-related biomarkers of AMI that could serve as diagnostic markers for the disease. Additionally, the predicted ceRNA network and drug interaction network associated with these genes offer new perspectives for the treatment of AMI.

Congenital heart defects (CHD) are internal risk factors that cause cardiac dysfunction. Maternal smoking is a cause of inducing CHD and cardiac dysfunction. Here, we aimed to investigate the influence of nicotine on fetal cardiac dysfunction and the underlying mechanism in mice. After maternal nicotine exposure (MNE), the female mice became pregnant, and the successful pregnancy rate was calculated. Fetal weight, cardiac function, and placental weight were measured at embryonic day 18.5. For in vitro experiments, primary cardiomyocytes were isolated. Cell apoptosis and inflammation were analyzed using flow cytometry and enzyme-linked immunosorbent assay. The molecular mechanism was evaluated using molecular docking, quantitative real-time PCR, and western blotting. The results showed that MNE reduced the fetal weight, cardiac function, and maternal pregnancy rate in vivo. Nicotine promotes apoptosis and inflammation of cardiomyocytes in vitro. Moreover, nicotine decreased KCTD10 expression and activated the Notch pathway. Inactivation of the Notch pathway using DAPT reversed the effects of nicotine on cardiomyocyte injury and MNE on fetal cardiac dysfunction. In conclusion, nicotine may promote fetal cardiac dysfunction by facilitating cardiomyocyte apoptosis through the KCTD10-Notch pathway.

This study explored the relationship among lncRNA NR_027324, miR-103-3p, and autophagy-related protein 5 (ATG5) in cardiomyocytes under hypoglycemic/hypoxic conditions.

Bioinformatics and luciferase assays were used to investigate the interaction between NR_027324 and miR-103-3p. H9C2 cells cultured under hypoglycemic/hypoxic conditions were transfected with NR_027324 siRNA, overexpression vectors, and miR-103-3p mimics/inhibitors. Cell viability and damage were measured using MTT and LDH assays, respectively. qRT-PCR was performed to assess the mRNA levels of NR_027324, miR-103a-3p, and ATG5. Protein expressions were analyzed by Western blotting, and immunofluorescence was used to observe LC3-I/II expression.

In hypoglycemic/hypoxic conditions, H9C2 cell viability decreased significantly, and LDH levels increased, indicating cell damage. Simultaneously, NR_027324 and ATG5 expressions were upregulated, while miR-103-3p was downregulated. Overexpression of NR_027324 enhanced cell viability and reduced LDH release. Conversely, knockdown of NR_027324 resulted in decreased cell viability and increased LDH release. In addition, knockdown of NR_027324 led to upregulation of miR-103-3p and downregulation of ATG5. Furthermore, the luciferase activity was significantly lower when miR-103-3p interacted with wildtype NR_027324, validating the binding between NR_027324 to miR-103-3p. The overexpression of NR_027324 led to downregulation of miR-103-3p, while its knockdown resulted in the upregulation of miR-103-3p. Lastly, NR_027324 overexpression alone significantly upregulated ATG5 expression, which was counteracted when NR_027324 and miR-103-3p were co-overexpressed.

The findings of this study highlight the significance of NR_027324, miR-103-3p, and ATG5 in mediating the autophagy and apoptosis response of H9C2 cells under hypoglycemic/hypoxic stress, providing valuable insights into potential targets for therapeutic interventions in related cardiovascular conditions.

We evaluated the effect of acute hypobaric hypoxia (AHH) on the heart of early-stage spontaneously hypertensive male rats (SHRs). The rats were classified into a control (ground level; ~400 m altitude) group and an SHR-AHH experimental group placed in an animal hypobaric chamber at a simulated altitude of 5500 m for 24 hours (24h).

RNA-Seq analysis of the hearts showed that differentially expressed genes (DEGs) were primarily associated with cellular processes, binding, and cell parts. KEGG enrichment analysis revealed that the DEGs were linked to the NOD-like receptor signaling pathway, MAPK signaling pathway, and metabolic pathways. Protein-protein interaction network analysis revealed that 165 DEGs were implicated in energy metabolism. Subsequently, we performed validation experiments to show that 8 DEGs were closely associated with energy metabolism. Among these genes, Ccna2, Cdc20, Prc1, Kif11, Kif20a, Ube2c, and Melk exhibited downregulated expression, while Cenpa exhibited upregulated expression.

Collectively, these results indicated that energy metabolism-associated gene expression in the heart was altered in early-stage hypertension upon AHH exposure.

Increasingly evidence suggests that microRNA (miRNA) plays a pivotal role in coronary artery disease (CAD). This study investigated the abundance of miR-4429 in the serum of CAD patients and explored the function of miR-4429 and its target GNAI2.

A total of 164 participants were enrolled. The relative expression levels of miR-4429 were quantified by qRT-PCR. The diagnostic performance and risk factors were analyzed using receiver operating characteristic (ROC) curves and binomial logistic regression (LR). Proliferation and apoptosis were assayed by CCK-8 and flow cytometry in human umbilical vein endothelial cells (HUVEC) induced by oxidized low-density lipoprotein (ox-LDL). The relationship between miR-4429 and GNAI2 was confirmed by dual-luciferase reporter assay and co-transfection.

miR-4429 levels were decreased and GNAI2 levels increased in CAD patient serum and ox-LDL-induced HUVEC. miR-4429 was negatively associated with white blood cells (WBC) and C-reactive protein (CRP). ROC curve analysis confirmed the efficacy of miR-4429 and GNAI2 in distinguishing CAD. miR-4429 and GNAI2 were independent predictors for CAD. Restoring miR-4429 reversed the ox-LDL-induced increases in IL-6, MCP-1, and ICAM-1, the suppression of HUVEC proliferation, and the promotion of apoptosis. GNAI2 was a direct target of miR-4429 by dual-luciferase assay. GNAI2 upregulation negated the suppression of cytokines and the protection of cellular function by miR-4429.

In summary, this study demonstrates the diagnostic value of miR-4429 and its association with serum inflammation levels in CAD. miR-4429 reversed ox-LDL-induced inflammatory-related cytokines, proliferation, and apoptosis in HUVEC, suggesting miR-4429 may serve as a protective biomarker by targeting the GNAI2 in CAD.

Patients with atherosclerosis obliterans (ASO) are at risk of amputation or even death if timely treatment is not provided; current clinical treatments for ASO have certain disadvantages. This study aimed to ascertain the function of miR-27b-3p in ASO to provide novel insights for ASO treatment.

The expression of miR-27b-3p in the serum of 117 ASO subjects and 80 healthy individuals was assessed by polymerase chain reaction. Risk factors for coronary artery disease (CAD) in ASO were assessed by multivariate logistic regression analysis. The atherosclerosis cell model was conducted using human vascular smooth muscle cells (HVSMCs) induced with oxidized low-density lipoprotein (ox-LDL). The interaction relationship between miR-27b-3p and GAB1 was assessed using a dual-luciferase reporter assay. HVSMC proliferation and migration were analyzed using the cell counting kit-8 and transwell assay.

MiR-27b-3p was upregulated in ASO; it was correlated with ASO severity indicators (ankle-brachial index level and Fontaine stage) and identified as a risk factor for CAD incidence in ASO. Ox-LDL induction in HVSMCs promoted HVSMC proliferation and migration. Overexpression of miR-27b-3p facilitated the proliferation and migration of ox-LDL-induced HVSMCs, which were attenuated by GAB1 overexpression.

The upregulation of miR-27b-3p in ASO was correlated with ASO severity and served as a risk factor for CAD in patients with ASO. The potential regulatory mechanism of miR-27b-3p in ASO was the acceleration of vascular smooth muscle cell proliferation and migration by targeting GAB1.

Heart failure (HF) is one of the most common cardiovascular diseases in the 21st century, affecting more than 25 million individuals worldwide. According to estimates, 8.9 million cases have been reported in China alone. Although pharmacotherapy remains an integral part of the treatment of HF, even with optimized medical treatment, many patients continue to experience symptoms and frequent rehospitalizations with a poor prognosis. This case series assessed the possible benefits of a left ventricular cardiac contractility modulation (CCM) device in 5 patients with chronic HF who had poor outcomes with medication alone. This study aimed to establish improvements caused by CCM in cardiac function and quality of life by analyzing variations in echocardiographic parameters, myocardial biomarkers, and exercise tolerance. Follow-ups at 1 and 6 months postoperatively showed equally impressive improvements in cardiac function, with equally dramatic improvements in quality of life.

Cardiac angiosarcoma is a rare malignant tumor with a poor prognosis. Because of its aggressive nature, early pathological diagnosis is essential. Previous studies have reported the efficacy of intracardiac echocardiography (ICE) -guided biopsy for unknown cardiac masses; however, its application is unclear. Herein, we describe a case of a giant cardiac angiosarcoma with extensive invasion, successfully diagnosed using ICE-guided biopsy. A 52-year-old man with palpitations and facial edema was admitted to our hospital. Contrast-enhanced computed tomography (CT) revealed a giant hypervascular tumor in the right atrium, extending into nearby structures, including the interatrial septum and left atrial roof. The tumor was initially suspected to be either a mediastinal tumor with cardiac invasion or a primary cardiac tumor. Given the high bleeding risk associated with percutaneous CT-guided or thoracoscopic biopsies, an ICE-guided biopsy of the right atrial mass was performed using a steerable sheath, without complications. The patient was diagnosed with angiosarcoma and underwent surgical resection. Intra-operative evaluation revealed that the tumor was confined to the pericardium with no mediastinal invasion, confirming the diagnosis of primary cardiac angiosarcoma. The patient underwent postoperative chemotherapy and radiotherapy, and is alive 7 months after surgery, demonstrating that ICE-guided biopsy using a steerable sheath is a safe and effective diagnostic tool for cardiac masses, particularly those with malignant characteristics and extensive invasion.