As atrial fibrosis is the main feature of atrial structural remodeling, inhibiting atrial fibrosis is crucial to the prevention of atrial fibrillation (AF) progression. Research has shown the correlation between abnormal lipid metabolism and AF progression. However, the effect of specific lipids on atrial fibrosis remains unclear. In the present study, we applied ultra-high-performance lipidomics to analyze the lipid profiles in patients with AF and identify phosphatidylethanolamine (PE) as the differential lipid associated with AF. To detect the effect of the differential lipid on atrial fibrosis, we performed the intraperitoneal injection of Angiotensin II (Ang II) to mice to induce atrial fibrosis and supplemented PE in diets. We also treated atrial cells with PE to evaluate the cellular effect of PE. We found that PE supplementation aggravated atrial fibrosis and increased the expression of the fibrosis-related protein in vitro and in vivo. Moreover, we detected the effect of PE on the atrium. We found that PE increased oxidation products and regulated the expression of ferroptosis-related proteins, which could be alleviated by a ferroptosis inhibitor. PE increased peroxidation and mitochondrial damage in vitro, which promoted cardiomyocyte death induced by Ang II. Examination of protein expression in cardiomyocytes indicated that PE triggered ferroptosis and caused cell death to participate in myocardium fibrosis. In summary, our findings demonstrated the differential lipid profiles of AF patients and revealed the potential effect of PE on atrial remodelling, suggesting that inhibition of PE and ferroptosis might serve as a potential therapy to prevent AF progression.

Objective. Adopting hearts from donation after circulatory death (DCD) is a promising approach to enlarge the donor pool. Nevertheless, DCD hearts experience severe warm ischemia/reperfusion (I/R) injury. Recent studies have demonstrated that conditioned medium (CM) derived from bone marrow mesenchymal stem cells (BMSCs) has the potential of reducing organ I/R injury. Therefore, we investigated whether DCD heart preservation with normothermic ex vivo heart perfusion (EVHP) and BMSCs-CM treatment could alleviate myocardial warm I/R injury in the DCD hearts. Methods. We randomly divided donor rats into two groups: (1) DCD-Control group and (2) DCD-CM group. Before DCD heart preservation with the normothermic EVHP system for 105 minutes, rats suffered from a 25-minute warm ischemia injury in the DCD procedure. Vehicle or CM (300 μl) was added to the perfusate at the beginning of the perfusion process. The cardiac function of DCD hearts in the DCD-Control and DCD-CM groups was measured every 30 minutes. Besides, non-DCD hearts were harvested from the beating-heart rats. Results. The antibody array demonstrated that the CM contained 14 bioactive factors involved in apoptosis, inflammation, and oxidative stress. Warm ischemia injury resulted in a significant increase in the level of oxidative stress, inflammation, and apoptosis in the DCD hearts of DCD-Control group. Furthermore, compared with the DCD-Control group, CM treatment increased the developed pressure, and of the left ventricular in the DCD hearts during a 90-minute EVHP. Moreover, the administration of CM attenuated the level of oxidative stress, inflammation, and apoptosis in the DCD hearts of the DCD-CM group. Conclusions. Normothermic EVHP combined with CM treatment can alleviate warm I/R injury in the DCD hearts by decreasing the level of oxidative stress, inflammatory response, and apoptosis, which might alleviate the shortage of donor hearts by adopting DCD hearts.

Sphingolipids (SLs) are vital constituents of the plasma membrane of animal cells and concurrently regulate numerous cellular processes. An escalating number of research have evinced that SLs assume a crucial part in the progression of tissue fibrosis, a condition for which no efficacious cure exists as of now. Cardiac fibrosis, and in particular, atrial fibrosis, is a key factor in the emergence of atrial fibrillation (AF). AF has become one of the most widespread cardiac arrhythmias globally, with its incidence continuing to mount, thereby propelling it to the status of a major public health concern. This review expounds on the structure and biosynthesis pathways of several pivotal SLs, the pathophysiological mechanisms of AF, and the function of SLs in cardiac fibrosis. Delving into the influence of sphingolipid levels in the alleviation of cardiac fibrosis offers innovative therapeutic strategies to address cardiac fibrosis and AF.

Objective: The present study aimed to investigate the association of postoperative central venous pressure (CVP) with acute kidney injury (AKI) and mortality in patients undergoing coronary artery bypass grafting (CABG).Method: Patients who underwent CABG in the MIMIC-III database were included and divided into two groups according to the optimal cutoff value of CVP for postoperative AKI determined by the receiver operating characteristic (ROC) curves. The association of CVP with AKI and mortality was determined by multivariate regression models. A 1:1 propensity score matching (PSM) was performed to balance the influence of potential confounding factors.Results: A total of 3,564 patients were included and divided into High CVP group (CVP ≥ 10.9 mmHg) and Low CVP group (CVP < 10.9 mmHg) according to the ROC analysis. Patients in High CVP group presented with higher AKI incidence (420 (28.2%) vs. 349 (16.8), p < 0.001), in-hospital mortality (28 (1.9%) vs. 6 (0.3%), p < 0.001) and 4-year mortality (149 (15.8%) vs. 162 (11.1%), p = 0.001). Multivariate regression model showed that CVP was an independent risk factor for the postoperative AKI (OR: 1.071 (1.035, 1.109), p < 0.001), in-hospital mortality (OR: 1.187 (1.026, 1.373), p = 0.021) and 4-year mortality (HR: 1.049 (1.003, 1.096), p = 0.035). A CVP above 10.9 mmHg was significantly associated with about 50% higher risk of AKI (OR: 1.499 (1.231, 1.824), p < 0.001). After PSM, 1004 pairs of score-matched patients were generated. The multivariate logistic model showed that patients with CVP ≥ 10.9 mmHg had a significantly higher risk of AKI (OR: 1.600 (1.268, 2.018), p < 0.001) in the PSM subset. However, CVP, as a continuous or a dichotomic variable, was not independently associated with in-hospital mortality (OR: 1.202 (0.882, 1.637), p = 0.244; OR: 2.636 (0.399, 17.410), p = 0.314) and 4-year mortality (HR: 1.030 (0.974, 1.090), p = 0.297; HR: 1.262 (0.911, 1.749), p = 0.162) in the PSM dataset.Conclusion: A mean CVP ≥ 10.9 mmHg within the first 24 h after CABG was independently associated with a higher risk of postoperative AKI.