Cardiovascular diseases (CVDs) remain the leading cause of mortality worldwide, driving the rapid advancement of cardiac tissue engineering (CTE) as a strategy to develop effective therapeutic interventions. Among its notable achievements is the cardiac patch, a supportive scaffold designed to repair damaged tissue following myocardial infarction (MI). This study selected alginate (Alg) due to its superior biocompatibility and printability for the fabrication of cardiac patches through extrusion-based 3D bioprinting, a novel technology for scaffold construction. To further enhance scaffold performance, graphene oxide (GO) nanosheets were incorporated into the Alg matrix to improve electrical conductivity, mechanical strength, cell adhesion, and printability. Bioinks comprising 8% Alg and different concentrations of GO (0, 0.05, 0.1, and 0.2 mg mL⁻¹) were formulated and thoroughly assessed for their physicochemical characteristics and cytocompatibility. All formulations exhibited suitable rheological characteristics for 3D printing. Moreover, the addition of GO reduced strand thickness, increased pore size, and improved overall printability. Mechanical testing revealed an increase in tensile strength from 0.18 MPa to 0.79 MPa with the addition of 0.2 mg mL⁻¹ of GO, while electrical conductivity reached (0.3 ± 0.00) × 10⁻⁶ S/m, approaching the range required for CTE. MTT assays demonstrated a concentration-dependent cytotoxic effect, showing decreased viability at 0.1 and 0.2 mg mL⁻¹ GO, while scaffolds with 0 and 0.05 mg mL⁻¹ GO preserved high viability. Scanning electron microscopy (SEM) further confirmed enhanced cell adhesion and filopodia extension in Alg-GO-1 (0.05 mg mL⁻¹) compared to pure Alg scaffolds. The findings generally suggested that Alg/GO composites, particularly at optimized concentrations, hold significant promise as bioinks for CTE due to their favorable mechanical, electrical, and biological properties.

Left ventricular thrombus (LVT) is a serious complication of anterior ST-elevation myocardial infarction (STEMI). Despite guideline endorsement of prophylactic anticoagulation in selected high-risk patients, the supporting evidence remains of low certainty. Aim of our systematic review and meta-analysis is to evaluate the efficacy and safety of triple antithrombotic treatment (TAT) versus dual antiplatelet treatment (DAPT) alone for LVT prevention in patients with anterior STEMI treated with primary percutaneous coronary intervention (pPCI). Three electronic databases (EMBASE, MEDLINE, Cochrane Library) were systematically searched from inception to February 2026, following PRISMA 2020 guidelines. Eligible studies enrolled adult patients with anterior STEMI revascularised by pPCI, compared prophylactic TAT with DAPT alone, and reported LVT outcomes. Data were pooled as risk ratios (RR) with 95% confidence intervals (CI) using random-effects models. The primary outcome was LVT formation; secondary outcomes were major bleeding and systemic embolism. Six studies including 2,021 patients were analyzed. Pooled analysis demonstrated no statistically significant reduction in LVT formation with TAT (RR 0.54, 95% CI 0.21-1.40; p=0.21; I2=61%), whereas major bleeding risk was significantly increased (RR 2.69, 95% CI 1.40-5.19; p=0.003; I2=14%). A non-significant trend toward reduced systemic embolism was observed (RR 0.44, 95% CI 0.18-1.07; p=0.07; I2=0%). The addition of prophylactic anticoagulation to DAPT in patients with anterior STEMI treated with pPCI does not show a statistically significant reduction in LVT formation while significantly increasing major bleeding risk. These findings do not support routine prophylactic TAT in unselected patients with anterior STEMI.

Myocardial infarction (MI) usually results in severe heart failure (HF), and patients suffer from the repercussions of MI, elucidation of the pathological basis of MI is crucial to optimize the prevention and treatment of MI. This study investigated the role of dysregulated circ_0001112 in MI. In our study, circ_0001112 was significantly upregulated in the MI model and by hypoxia treatment. Circ_0001112 overexpression inhibited hypoxia-induced cardiomyocyte apoptosis. Luciferase assay showed that circ_0001112 sponged miR-324-5p that regulated the expression of cyclin-dependent kinase 6 (CDK6). Ago2-miRNP immunoprecipitation further confirmed that the 3'-untranslated region (3'UTR) of CDK6 was targeted by miR-324-5p. Either miR-324-5p overexpression or CDK6 knockdown prevented cardiomyocyte apoptosis induced by circ_0001112 overexpression. In conclusion, this study demonstrated that the downregulation of circ_0001112 promoted cardiomyocyte apoptosis by sponging miR-324-5p and upregulating CDK6 expression in MI.

Cardiac fibrosis remains a critical determinant of adverse outcomes in heart disease, yet effective anti-fibrotic therapies are lacking. While multiple semaphorin family members participate in cardiovascular pathophysiology, the role of semaphorin 4f (Sema4f) in cardiac fibrosis remains unexplored. This study investigates the role and mechanisms of Sema4f in fibrotic remodeling post-myocardial infarction (MI). We employed flow cytometry to characterize cell type-specific Sema4f expression patterns in post-MI hearts. Lineage-specific knockout mice (fibroblast vs. myeloid) were subjected to left anterior descending ligation to assess functional consequences. Proteomic analysis of Sema4f-deficient cardiac fibroblasts was conducted to identify downstream effectors. Key pathways were subsequently validated using pharmacological inhibitors. We found that Sema4f expression was markedly upregulated during the fibrotic phase post-MI, primarily due to fibroblast activation. Fibroblast-, but not myeloid-, specific Sema4f deletion significantly reduced fibrosis and improved cardiac function. Proteomic profiling revealed that Sema4f deficiency led to downregulation of pro-fibrotic gene expression, which was associated with impaired actin cytoskeletal remodeling and decreased nuclear translocation of YAP/TAZ. Pharmacological inhibition of either actin remodeling or YAP/TAZ activity attenuated fibrosis, whereas YAP/TAZ activation abolished the anti-fibrotic effects of Sema4f knockout. Our study provides the first evidence demonstrating the functional role of Sema4f in cardiac fibroblast activation and fibrosis progression. We have identified a fibroblast-specific mechanism mediated by the Sema4f-actin cytoskeleton-YAP/TAZ axis, offering novel mechanistic insights into fibrosis regulation and revealing a promising therapeutic target for cardiac fibrosis with potential clinical applications.

Brain-heart syndrome (BHS) describes cardiac dysfunction secondary to central nervous system injury, with acute ischemic stroke (AIS) serving as a critical driver that exacerbates myocardial infarction (MI). This study aimed to elucidate the role of Apolipoprotein M (APOM) in stroke-aggravated MI and to explore its underlying systemic and molecular mechanisms. Clinical data were analyzed to evaluate the correlation between stroke and MI. A combined mouse model of middle cerebral artery occlusion (MCAO) and MI was established to assess neurological and cardiac injury. Quantitative proteomics and Weighted Gene Co-expression Network Analysis (WGCNA) were employed to screen key differentially expressed proteins. The role of APOM in myocardial injury was validated using APOM-knockout (KO) mice. Furthermore, nuclear-cytoplasmic fractionation, immunofluorescence, and Western blot were performed to investigate its effects on the Saa1 and NF-κB signaling, NLRP3-related inflammatory signaling pathway, and lipid metabolism pathways. Clinical analysis indicated that stroke is a significant risk factor for MI (OR = 4.5). In the mouse model, MCAO significantly exacerbated post-MI electrocardiographic abnormalities, myocardial inflammatory response, while elevating circulating levels of cTnT and IL-1β. Proteomics identified a significant downregulation of APOM in the heart, brain, and serum post-stroke, a trend consistent with observations in AIS patients. Further experiments revealed that APOM deficiency markedly worsened cardiac conduction disturbances, histological damage, and inflammatory responses in MI mice. Mechanistically, the loss of APOM upregulates the acute-phase protein Saa1, triggers NF-κB phosphorylation and nuclear translocation, and enhances inflammatory signaling related to inflammasomes, while simultaneously mediating cytokine release from cardiomyocytes. Concurrently, APOM deficiency led to a significant decrease in sphingosine-1-phosphate (S1P) and also caused myocardial lipid droplet accumulation and metabolite changes. Additionally, the loss of APOM increased the expression of D-dimer and fibrinogen family proteins. Our findings suggest that APOM is a potential cardioprotective agent post-AIS. Downregulation of APOM may exacerbate myocardial injury after MI by elevating Saa1 expression, activating the NF-κB pathway and the inflammasome-mediated signaling, and inducing lipid metabolic disorders and coagulation-associated alterations. APOM may represent a potential therapeutic target for the intervention of brain-heart syndrome.

Obesity rates have increased dramatically during the past four decades, and these increases have occurred in children and adolescents, as well as in adults at reproductive age. Currently, 40.3% of men and 39.7% of women 20-39 years of age in the United States are classified as obese, leading to a substantial rise in parental obesity. Obesity is a major risk factor for cardiovascular, metabolic and renal diseases, including hypertension, type 2 diabetes, and chronic kidney diseases. This review examines current evidence of how parental obesity programs offspring susceptibility to cardiorenal and metabolic dysfunction and discusses the potential underlying mechanisms that contribute to the long-term health consequences in the offspring.

Autonomic nervous system (ANS) imbalance, characterized by chronic sympathetic overactivity and diminished parasympathetic tone, has increasingly been recognized as an important contributor to the pathogenesis of myocardial infarction [1-3]. ANS dysfunction not only affects hemodynamics directly, but also triggers a harmful chain of events. These include insulin resistance, the renin angiotensin aldosterone system (RAAS) activation, systemic inflammation, and endothelial dysfunction [4-6]. Crucially, ANS dysregulation often manifests as a spectrum of prodromal symptoms including altered heart rate variability (HRV), blood pressure lability, visceral discomfort, and functional pain syndromes which provide an identifiable clinical window for early intervention. Targeted modulation of the ANS has thus emerged as a promising strategy for primary prevention [7, 8]. Among non-invasive approaches, photobiomodulation (PBM), particularly in the form of laser acupuncture, represents a novel neuromodulatory tool capable of rebalancing autonomic function [9, 10]. PBM acts through dual pathways: peripherally, by stimulating sensory afferents to reflexively modulate autonomic output, and centrally, by enhancing mitochondrial function, reducing neuroinflammation, and promoting neural plasticity within key brainstem and hypothalamic regulatory centers. These mechanisms may translate into measurable improvements in HRV, reductions in heart rate and blood pressure, attenuation of inflammatory markers, and enhanced vascular function [11,12]. This review proposes autonomic dysfunction as a potential modifiable preclinical window for myocardial infarction (MI) prevention. It positions photobiomodulation (PBM) as a systems-level, non-invasive strategy for autonomic rebalancing and cardiovascular risk reduction, warranting future prospective validation and protocol optimization.

BackgroundAlthough an association between carfilzomib and cardiovascular adverse events has been well documented, the risk factors for carfilzomib-induced cardiovascular adverse events in the Chinese population remain unclear. This study aimed to evaluate the incidence of and identify the risk factors for cardiovascular adverse events associated with carfilzomib in Chinese patients with multiple myeloma in a real-world setting.MethodsWe conducted a real-world retrospective cohort study of cardiovascular adverse events in patients with multiple myeloma treated with carfilzomib at Tianjin First Central Hospital between August 2022 and April 2026. Cardiovascular adverse events included severe hypertension, arrhythmia, heart failure, venous thromboembolism, myocardial infarction, and angina. Multivariable logistic regression was performed to identify risk factors for the development of cardiovascular adverse events during carfilzomib therapy.ResultsAmong the 74 enrolled patients, 36 (48.6%) developed cardiovascular adverse events during carfilzomib therapy. The median time from treatment initiation to the first cardiovascular adverse event was 56 days (range, 4-559), with 67% (24/36) occurring within the first 3 months. Severe hypertension was the most common cardiovascular complication, accounting for 50% of all cardiovascular adverse events, followed by arrhythmia (47%). Multivariable analysis identified elevated baseline N-terminal pro-B-type natriuretic peptide levels as an independent predictor of subsequent carfilzomib-related cardiovascular adverse events (odds ratio, 6.16; P = 0.002).ConclusionsCardiovascular adverse events occur frequently during carfilzomib therapy in Chinese patients with multiple myeloma. Elevated baseline N-terminal pro-B-type natriuretic peptide levels may serve as an important biomarker for predicting the risk of cardiotoxicity. Patients at high risk, particularly those with elevated baseline N-terminal pro-B-type natriuretic peptide levels, may therefore require close cardiovascular monitoring throughout the course of carfilzomib treatment.