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The global incidence and prevalence of arrhythmias are continuously increasing. However, the precise mechanisms of underlying arrhythmogenesis and the optimal measures for effective treatment remain incompletely understood. The inducible form of heme oxygenase, known as heme oxygenase-1 (HO-1), is recognized as a potent antioxidant molecule capable of exerting anti-inflammatory and anti-apoptotic effects. Recent research indicates that HO-1 plays a role in preventing arrhythmias by mitigating cardiac remodeling, including electrical remodeling, ion remodeling, and structural remodeling. This review aimed to consolidate current knowledge regarding the involvement of HO-1 in arrhythmias and elucidate its underlying mechanisms of action. [ABSTRACT FROM AUTHOR]

Ventricular arrhythmias are the leading cause of sudden cardiac death in patients after myocardial infarction (MI). Connexin43 (Cx43) is the most important gap junction channel-forming protein in cardiomyocytes. Dysfunction of Cx43 contributes to impaired myocardial conduction and the development of ventricular arrhythmias. Following an MI, Cx43 undergoes structural remodeling, including expression abnormalities, and redistribution. These alterations detrimentally affect intercellular communication and electrical conduction within the myocardium, thereby increasing the susceptibility to post-infarction ventricular arrhythmias. Emerging evidence suggests that post-translational modifications play essential roles in Cx43 regulation after MI. Therefore, Cx43-targeted management has the potential to be a promising protective strategy for the prevention and treatment of post infarction ventricular arrhythmias. In this article, we primarily reviewed the regulatory mechanisms of Cx43 mediated post-translational modifications on post-infarction ventricular arrhythmias. Furthermore, Cx43-targeted therapy have also been discussed, providing insights into an innovative treatment strategy for ventricular arrhythmias after MI. [ABSTRACT FROM AUTHOR]

Dilated cardiomyopathy (DCM) is characterized by the left ventricular dilatation and impaired myocardial systolic dysfunction with high mortality and morbidity. However, the underlying mechanisms remain elusive. We first identified the differentially expressed genes (DEGs) between the DCM and control group using two expression profiles from GSE3585 and GSE84796. Enrichment analysis was conducted to explore the potential mechanisms underlying DCM. A total of four algorithms, including key module of MCODE, degree, maximum neighborhood component (MNC), and maximal clique centrality (MCC), were used to identify the hub genes within Cytoscape. The correlation between hub genes and infiltrated immune cells was evaluated to determine potential immune-related genes. The expression analysis and diagnosis value analysis of potential immune-related genes were performed. Finally, the expression analysis with GSE57338 and relationship analysis with the comparative toxicogenomics database (CTD) were performed to identify the key immune-related genes in DCM. A total of 80 DEGs were screened for DCM. Enrichment analysis revealed that DEGs were involved in the immune-related pathological process. Immune infiltration analysis indicated a potentially abnormal immune response in DCM. Four up-regulated genes (COL1A2, COL3A1, CD53, and POSTN) were identified as potential immune-related genes. Finally, three genes (COL1A2, COL3A1, and POSTN) were determined as the key immune-related genes in DCM via expression analysis with a validation set (GSE57338) and relationship analysis with CTD. Our study suggested that the upregulated COL1A2, COL3A1, and POSTN might be the key immune-related genes for DCM. Further studies are needed to validate the underlying mechanisms. [ABSTRACT FROM AUTHOR]

These authors contributed equally: Feng Li, Tong-Yue Du and Li-Da Wu. Correction to: I Scientific Reports i https://doi.org/10.1038/s41598-022-26277-w, published online 01 February 2023 The original version of this Article contained an error in the order of the author names, which was incorrectly given as Feng Li, Tong-Yue Du, Li-Da Wu, Lei Zhang, Huan-Huan Liu, Zhen-Ye Zhang, Jie Zhang, Zhi-Yuan Zhang, Ling-Ling Qian, Jian-Feng Hao & Ru-Xing Wang. [Extracted from the article]

Background: There are no reports regarding entire gastric fundic and esophageal varices evaluated with 64-row multidetector CT (MDCT). We attempt to clarify the feasibility of portal venography with this scanner in evaluation of these varices. Methods: A total of 33 patients, with clinically confirmed gastric fundic and esophageal varices secondary to posthepatitic cirrhosis, underwent thoracicoabdominal triphasic enhancement scans using 64-row MDCT along with conventional angiographic portography. CT portography and conventional portography were compared by statistical agreement to determine whether CT maximum intensity projection (CT-MIP) portography is useful in evaluation of entire gastric fundic and esophageal varices. Results: CT-MIP portography demonstrated gastric fundic and esophageal varices, and the inflowing and outflowing vessels of the varices. Gastric fundic varices were shown in 32 cases (97.0%), and esophageal varices were in 27 (81.8%). The inflowing vessels including the left gastric vein and posterior gastric vein/short gastric vein were illustrated in 31 (94.0%) and 17 (51.5%) cases, respectively. The outflowing vessels including the azygos vein, hemiazygos vein, and gastro-renal shunts were seen in 30 (90.9%), 8 (24.2%), and 12 (36.4%) cases, respectively. Findings of CT-MIP portography and conventional angiographic portography were in close agreement (Kappa value ranged from 0.621 to 1.000). Conclusion: CT-MIP venography with 64-row MDCT could be considered as a method for detecting entire gastric fundic and esophageal varices developed from posthepatitic cirrhosis. [ABSTRACT FROM AUTHOR]