Broadening horizons: The role of ferroptosis in myocardial ischemia-reperfusion injury.

Ferroptosis is a novel type of regulated cell death (RCD) discovered in recent years, where abnormal intracellular iron accumulation leads to the onset of lipid peroxidation, which further leads to the disruption of intracellular redox homeostasis and triggers cell death. Iron accumulation with lipid peroxidation is considered a hallmark of ferroptosis that distinguishes it from other RCDs. Myocardial ischemia-reperfusion injury (MIRI) is a process of increased myocardial cell injury that occurs during coronary reperfusion after myocardial ischemia and is associated with high post-infarction mortality. Multiple experiments have shown that ferroptosis plays an important role in MIRI pathophysiology. This review systematically summarized the latest research progress on the mechanisms of ferroptosis. Then we report the possible link between the occurrence of MIRI and ferroptosis in cardiomyocytes. Finally, we discuss and analyze the related drugs that target ferroptosis to attenuate MIRI and its action targets, and point out the shortcomings of the current state of relevant research and possible future research directions. It is hoped to provide a new avenue for improving the prognosis of the acute coronary syndrome.

Expressions of serum adiponectin and visfatin in patients with hypertension in cerebrovascular accidents and analysis of risk factors.

OBJECTIVE: To determine the expressions of serum adiponectin and visfatin in patients with hypertension and cerebrovascular accidents and to analyze the risk factors. METHODS: Data of 161 patients with hypertension treated in The Affiliated Hospital of Shandong University of Traditional Chinese Medicine from March 2019 to July 2021 were retrospectively analyzed. There were 72 patients with cerebrovascular accidents assigned to an occurrence group. The remaining 89 patients without cerebrovascular accidents were assigned to a non-occurrence group. The two groups were compared in terms of the coagulation function (activated partial thromboplastin time, prothrombin time, and fibrinogen), liver function (aspartate aminotransferase (AST), glutamic pyruvic transaminase (GPT), albumin and total bilirubin (TB)), blood lipid indexes (cholesterol, triglyceride, high-density lipoprotein (HDL), low-density lipoprotein (LDL)), serum adiponectin, and visfatin levels. Pearson's correlation coefficient was performed to analyze the correlation of serum adiponectin and visfatin with blood lipid indexes. Logistics regression was performed to analyze the risk factors of stroke in patients with hypertension. RESULTS: The two groups were similar in terms of sex, age, education level, smoking, drinking, and diabetes histories (P>0.05). There were more patients ≥65 years old with body mass index ≥20 kg/m2 and with hyperlipidemia in the occurrence group than those in the non-occurrence group (P<0.05). The two groups were not notably different in activated partial thromboplastin time, prothrombin time, fibrinogen, AST, GPT, albumin, TB, total cholesterol, and HDL (P>0.05). The occurrence group showed significantly higher triglyceride, LDL and adiponectin levels, and a notably lower visfatin level than the non-occurrence group (P<0.05). Adiponectin showed a positive correlation with triglyceride and a negative association with LDL (P<0.05). Visfatin showed only a negative correlation with triglyceride (P<0.05), but no correlation with LDL (P>0.05). A multivariate logistics regression analysis reported that hyperlipidemia, triglyceride, LDL, adiponectin, and visfatin were independent risk factors for stroke in patients with hypertension (P<0.05). CONCLUSION: Serum adiponectin and visfatin were differentially expressed in patients with both hypertension and stroke. Our regression analysis revealed that serum adiponectin and visfatin were independent risk factors for stroke in patients with hypertension.

Metabolic status and vascular endothelial structure in obese hypertensive patients treated with non-pharmacological therapies: A systematic review and meta-analysis.

OBJECTIVE: This meta-analysis aimed to evaluate the efficacy of non-drug treatment on metabolism and vascular endothelium in obese hypertension. METHODS: Relevant publications were searched in the PubMed, Embase, and Cochrane Library databases for clinical studies on the effects of non-pharmacological treatments in obese hypertensive patients published from inception to April 2022. After searching and screening the literature, information was extracted, and the quality of the literature was evaluated by the investigators. Data processing was performed using Rev Man 5.3 statistical analysis software, while the TSA 0.9 software was used for sequential analysis of blood pressure and endothelial-related indicators. RESULTS: A total of 8 literature articles with 480 patients were included. The analysis showed that non-pharmacological treatment effectively reduced systolic blood pressure, diastolic blood pressure, heart rate, body weight, body mass index, glucose levels, soluble intercellular adhesion molecule 1, triglycerides, triglycerides, Low-density lipoprotein. For tumor necrosis factor α, soluble vascular cell adhesion molecule 1, high-density lipoprotein, C-reactive protein, high-sensitive C-reactive protein, and total antioxidant status by dietary supplements mainly. In contrast, no significant treatment effect was observed for Endothelin-1. Sequential analysis of the trial showed definitive evidence for improvement in blood pressure and inflammation. CONCLUSION: Non-pharmacological treatment of obese hypertensive patients may reduce blood pressure, body weight, and blood glucose, control inflammatory factor release and improve vascular endothelium to some extent.

Protective Effect of Trimetazidine on Potassium Ion Homeostasis in Myocardial Tissue in Mice with Heart Failure.

The occurrence of heart failure (HF) is closely correlated with the disturbance of mitochondrial energy metabolism, and trimetazidine (TMZ) has been regarded as an effective agent in treating HF. Intracellular potassium ion (K+) homeostasis, which is modulated by K+ channels and transporters, is crucial for maintaining normal myocardial function and can be disrupted by HF. This study is aimed at exploring the protective effect of TMZ on K+ homeostasis within myocardial tissue in mice with HF. We observed the pathological changes of myocardial tissue under microscopes and further measured the content of adenosine triphosphate (ATP), the activity of Na+-K+ ATPase, and the expression of ATP1α1 at the mRNA and protein levels. Moreover, we also analyzed the changes in K+ flux across the myocardial tissue in mice. As a result, we found that there was a large amount of myocardial fiber lysis and fracture in HF myocardial tissue. Meanwhile, the potassium flux of mice with HF was reduced, and the expression of ATP1α1, the activity of Na+-K+ ATPase, and the supply and delivery of ATP were also decreased. In contrast, TMZ can effectively treat HF by restoring K+ homeostasis in the local microenvironment of myocardial tissues.

Integrated bioinformatic analysis of microarray data reveals shared gene signature between MDS and AML.

Myeloid disorders, especially myelodysplastic syndrome (MDS) and acute myeloid leukemia (AML), cause significant mobility and high mortality worldwide. Despite numerous attempts, the common molecular events underlying the development of MDS and AML remain to be established. In the present study, 18 microarray datasets were selected, and a meta-analysis was conducted to identify shared gene signatures and biological processes between MDS and AML. Using NetworkAnalyst, 191 upregulated and 139 downregulated genes were identified in MDS and AML, among which, PTH2R, TEC, and GPX1 were the most upregulated genes, while MME, RAG1, and CD79B were mostly downregulated. Comprehensive functional enrichment analyses revealed oncogenic signaling related pathway, fibroblast growth factor receptor (FGFR) and immune response related events, 'interleukine-6/interferon signaling pathway, and B cell receptor signaling pathway', were the most upregulated and downregulated biological processes, respectively. Network based meta-analysis ascertained that HSP90AA1 and CUL1 were the most important hub genes. Interestingly, our study has largely clarified the link between MDS and AML in terms of potential pathways, and genetic markers, which shed light on the molecular mechanisms underlying the development and transition of MDS and AML, and facilitate the understanding of novel diagnostic, therapeutic and prognostic biomarkers.