Introduction: Myeloid differentiation protein 1 (MD1), a negative regulator of toll-like receptor 4 (TLR4), is widely expressed in the heart. Recent studies have shown that MD1 plays an important role in cardiac remodelling. However, the effects and potential mechanisms underlying MD1-mediated atrial remodelling in diabetic cardiomyopathy (DCM) remain unclear. Therefore, this study was designed to explore the role of MD1 in DCM-related atrial remodelling. Methods: MD1 knockout (MD1-KO) mice and wild-type (WT) littermates were injected with streptozotocin (STZ) to establish a diabetic mouse model. These mice were then used to evaluate MD1 expression and its effects on atrial remodelling in vivo. Results: MD1 expression was significantly decreased in STZ-induced diabetic mice. The loss of MD1 aggravated atrial fibrosis, inflammation, and apoptosis in DCM mice and promoted atrial remodelling. MD1-KO diabetic mice also showed higher susceptibility to atrial fibrillation (AF) and worse cardiac function. Mechanistically, the deletion of MD1 promoted the activation of the TLR4/NF-κB signalling pathway, resulting in atrial remodelling in DCM mice via increased p65 phosphorylation. Conclusions: The deletion of MD1 plays an important role in inflammatory and apoptotic atrial remodelling and increases susceptibility to AF in DCM mice, providing a new target for the preventive treatment of DCM-related atrial remodelling.

Introduction: The triglyceride–glucose (TyG) index has been closely associated with a range of cardiovascular diseases. However, the association between the TyG index and left ventricular aneurysm (LVA) formation in patients with acute ST-segment elevation myocardial infarction (STEMI) who underwent primary percutaneous coronary intervention (PCI) remains unknown. Methods: This study recruited 551 patients in the first cohort and 471 patients in the validation cohort. To determine the independent risk factors associated with LVA formation, a multivariable logistic regression analysis was conducted. The predictive capability of both the TyG index and the composite variable for LVA formation was evaluated through the use of ROC curve analysis. Results: The prevalence of LVA was found to be 14.5% in the first cohort and 13.6% in the validation cohort. In both cohorts, a higher TyG index correlated with an increased incidence of LVA (20.5% vs. 8.0%, P < 0.001 in the first cohort; 18.4% vs. 8.6%, P = 0.002 in the validation cohort). The TyG index was consistently elevated in the LVA group in comparison to those without LVA (9.3 ± 0.7 vs. 8.9 ± 0.9, P < 0.001 in the first cohort; 9.4 ± 0.7 vs. 9.0 ± 0.7, P < 0.001 in the validation cohort). Analysis using multivariable logistic regression showed that an independent relationship exists between the TyG index and the risk of LVA in both the first (OR = 4.2, P = 0.004) and validation (OR = 2.11, P = 0.008) cohorts. The applicability of the TyG index in predicting LVA had C statistics of 0.736 for the first cohort and 0.738 for the validation cohort, which surpassed those of triglycerides and fasting plasma glucose. The composite variable consisting of the TyG index, left ventricular ejection fraction, and left anterior descending artery (LAD) as the culprit vessel significantly improved the discriminant power (C statistic = 0.913 in the first cohort and 0.89 in the validation cohort). Discussion: A higher TyG index was independently linked to the development of LVA in patients with acute STEMI who received primary PCI.