Under the long‐term pressure overload stimulation, the heart experiences embryonic gene activation, leading to myocardial hypertrophy and ventricular remodelling, which can ultimately result in the development of heart failure. Identifying effective therapeutic targets is crucial for the prevention and treatment of myocardial hypertrophy. Histone lysine lactylation (HKla) is a novel post‐translational modification that connects cellular metabolism with epigenetic regulation. However, the specific role of HKla in pathological cardiac hypertrophy remains unclear. Our study aims to investigate whether HKla modification plays a pathogenic role in the development of cardiac hypertrophy. The results demonstrate significant expression of HKla in cardiomyocytes derived from an animal model of cardiac hypertrophy induced by transverse aortic constriction surgery, and in neonatal mouse cardiomyocytes stimulated by Ang II. Furthermore, research indicates that HKla is influenced by glucose metabolism and lactate generation, exhibiting significant phenotypic variability in response to various environmental stimuli. In vitro experiments reveal that exogenous lactate and glucose can upregulate the expression of HKla and promote cardiac hypertrophy. Conversely, inhibition of lactate production using glycolysis inhibitor (2‐DG), LDH inhibitor (oxamate) and LDHA inhibitor (GNE‐140) reduces HKla levels and inhibits the development of cardiac hypertrophy. Collectively, these findings establish a pivotal role for H3K18la in pathological cardiac hypertrophy, offering a novel target for the treatment of this condition.

Pulmonary arterial hypertension (PAH) is a severe disease resulting from progressive increases in pulmonary vascular resistance and pulmonary vascular remodeling, ultimately leading to right ventricular failure and even death. Hypoxia, inflammation, immune reactions, and epigenetic modifications all play significant contributory roles in the mechanism of PAH. Increasingly, epigenetic changes and their modifying factors involved in reprogramming through regulation of methylation or the immune microenvironment have been identified. Among them, histone lactylation is a new post-translational modification (PTM), which provides a novel visual angle on the functional mechanism of lactate and provides a promising diagnosis and treatment method for PAH. This review detailed introduces the function of lactate as an important molecule in PAH, and the effects of lactylation on N6-methyladenosine (m⁶A) and immune cells. It provides a new perspective to further explore the development of lactate regulation of pulmonary hypertension through histone lactylation modification.

Myocarditis is a complex disease characterized by myocardial inflammatory cell infiltration. The purpose of our study was to investigate the gene and single-cell signature to explore the involvement of immune cells in myocarditis. Gene expressions merged from GSE35182 and GSE35182 datasets were subjected to differential expression gene (DEG) analysis and PPI network construction. The correlation analysis of DEGs with immune cell infiltration was performed. Single-cell RNA sequencing (scRNA-seq) was downloaded from GSE174458. A total of 58 DEGs were identified, including 51 DEGs upregulated and 7 DEGs downregulated in the myocarditis group compared with the control group. GO and KEGG enrichment analyses revealed that myocarditis triggered DEGs mainly involved in immune-related processes and pathways. PPI network analysis identified 20 central hub genes. Occurrence of myocarditis induced significant enrichment of conventional dendritic cell 2 (cDC2), plasmacytoid DC, and plasma cell in myocardial tissue. Mmp12, Gpnmb, and Atp6v0d2 expressions were positively correlated with cDC abundance, of which only Mmp1 and Gpnmb were shared with hub gene list. A total of 20972 cells in scRNA-seq yielded 26 cell clusters and annotated 9 cell types, including fibroblasts, neutrophils, stromal cells, monocytes, basophils, B cells, natural killer T cells, innate lymphoid cells, and T cells, and only proportion of natural killer T cells and monocytes were higher in the myocarditis than in control. Monocytes annotated 3 subclusters including DC, macrophage, and monocytes. Hub genes of Ctss, Mpeg1, Cybb, H2-Ab1, Ly86, CD74, and Lgals3 were highly expressed in monocytes cluster. Among DC-correlated DEGs, Mmp12 was mainly expressed in monocyte cluster, and Gpnmb was mainly expressed in fibroblast cluster, whereas Atp6v0d2 expression has a weaker signal and weaker cell preference. In conclusion, DC infiltration and its associated pivotal genes may be responsible for progression of myocarditis. Our study expands and provides novel information on the immune cell engagement of myocarditis.

Background: Ventricular septal defect (VSD) and atrial septal defect (ASD) are congenital heart diseases. The techniques of transthoracic closure (TC) and percutaneous closure (PC) for the treatment of VSD and ASD have continuously improved and matured. This study aimed to retrospectively analyze the therapeutic effects of TC and PC on VSD and ASD patients. Methods: We retrospectively reviewed 928 patients (552 VSD and 376 ASD) who had undergone TC or PC guided by transesophageal ultrasound at the Department of Cardiac Macrovascular Surgery of the First Affiliated Hospital of Nanchang University between August 2010 and August 2020. We collected and evaluated the clinical data of the patients, including age, gender, weight, inlet and outlet diameters of defect, and the operation results of TC and PC. Descriptive statistics were used to analyze means and standard deviations (SD), and the Chi-square test was used to evaluate the difference between groups. Results: Among the 928 patients who were treated with the closure operation, there were no casualties, with 907 patients (97.7%) showing successful closure. Among the 552 VSD patients who were treated with TC, 540 showed successful close, while 12 cases required extracorporeal circulation after the failure of TC. Among the 376 patients with ASD, 256 patients were treated with TC, of which 251 were successful, and five were failures, including three shedding cases. In addition, among the 120 patients who were treated with PC, 116 were successful, and four were failures, including two shedding cases. Postoperative follow up for patients with successful closure operations demonstrated that the complications of aortic and tricuspid regurgitation, hydro-pericardium, III° atrioventricular block, shedding of closure umbrella, hemolysis, and thrombosis had not occurred. Conclusion: Closure operation of VSD and ASD by esophageal ultrasound has the advantages of lower trauma and blood loss, shorter hospital stay, simple operation, fewer postoperative complications, and significant therapeutic efficacy.

Cover: The cover image, by Zhou et al, is based on the Research Article, Notch signaling promotes angiogenesis and improves cardiac function after myocardial infarction, DOI: 10.1002/jcb.27032