Ferroptosis is a newly discovered form of regulated cell death dependent on iron and reactive oxygen species (ROS). It directly or indirectly affects the activity of glutathione peroxidases (GPXs) under the induction of small molecules, causing membrane lipid peroxidation due to redox imbalances and excessive ROS accumulation, damaging the integrity of cell membranes. Ferroptosis is mainly characterized by mitochondrial shrinkage, increased density of bilayer membranes, and the accumulation of lipid peroxidation. Myocardial ischemia‐reperfusion injury (MIRI) is an unavoidable risk event for acute myocardial infarction. Ferroptosis is closely associated with MIRI, and this relationship is discussed in detail here. This review systematically summarizes the process of ferroptosis and the latest research progress on the role of ferroptosis in MIRI to provide new ideas for the prevention and treatment of MIRI.

Purpose: Myocardial ischemia-reperfusion injury (MIRI) is a common pathophysiological process after occlusion of the blood vessels to restore blood supply. Apoptosis is one of the ways of myocardial cell death in this process. MicroRNAs (miRNAs), a class of short and noncoding RNAs, are involved in multiple biological processes by post-transcriptionally targeting their downstream effectors. To date, whether miRNAs exert biological effects in myocardial ischemia-reperfusion (I/R) injury remains to be further studied. Methods: In this study, we induced MIRI model by ligating rat left anterior descending artery (LAD) for 30 mins and reperfusion for 2 hrs. The differential expression profile of miRNAs in rat models of MIRI was analyzed by miRNAs sequencing. Results: We found that miRNAs sequencing analysis showed the expressions of 15 types of miRNAs, including miR-346, were downregulated and 29 types of miRNAs were elevated in the MIRI rat model. We observed the key regulator of apoptosis Bax was a predicted downstream target of miR-346 using online software TargetScan. And luciferase reporter assay was utilized to certify this prediction. Over-expression of miR-346 can attenuate myocardial injury and narrow infarct area by inhibiting myocardial cell apoptosis in rat models. Conclusion: This study revealed a novel pathway, miR-346/Bax axis, in the regulation of apoptosis in MIRI and which might be a new molecular mechanism and therapeutic target.

Purpose. Studies have found that microRNAs (miRNAs) are closely associated with atrial fibrillation, but their specific mechanism remains unclear. The purpose of this experiment is to explore the function of miR‐29b‐3p in regulating atrial remodeling by targeting PDGF‐B signaling pathway and thereby also explore the potential mechanisms. Methods. We randomly divided twenty‐four rats into four groups. Caudal intravenous injections of angiotensin‐II (Ang‐II) were administered to establish atrial fibrosis models. Expressions of miR‐29b‐3p and PDGF‐B were then tested via RT‐PCR, western blot, and immunohistochemistry. Binding sites were then analyzed via the bioinformatics online software TargetScan and verified by Luciferase Reporter. We used Masson staining to detect the degree of atrial fibrosis, while immunofluorescence and western blot were used to detect the expressions of Collagen‐I and a‐SMA. We used immunohistochemistry and western blot to detect the expression of connexin 43 (Cx43). Results. In comparison with the Ang‐II group, miR‐29b‐3p was seen to lower the degree of atrial fibrosis, decrease the expression of fibrosis markers such as Collagen‐I and a‐SMA, and increase the protein expression of Cx43. MiR‐29b‐3p can lower the expression of PDGF‐B, while the Luciferase Reporter showed that PDGF‐B is the verified target gene of miR‐29b‐3p. Conclusions. MiR‐29b‐3p was able to reduce atrial structural and electrical remodeling in the study’s rat fibrosis model. This biological function may be expressed through the targeted regulation of the PDGF‐B signaling pathway.

Objective. To perform a systematic evaluation of the efficacy and safety of combined treatment of Shenmai injection and chemotherapy for lung cancer. Methods. A literature search for randomized controlled trials (RCTs) describing the treatment of lung cancer by Shenmai injection and chemotherapy or chemotherapy alone was performed using the PubMed, Cochrane Library, China National Knowledge Infrastructure (CNKI), Value In Paper (VIP), China BioMed, and Wanfang databases. The databases were searched for entries published before September 1, 2019. Results. Thirty-seven RCTs, comprising a total of 2808 cases, were included in the present meta-analysis. Of these, 1428 cases were treated by Shenmai injection plus chemotherapy, and 1380 cases were treated only by chemotherapy. The results of meta-analysis showed that the combined treatment (Shenmai injection plus chemotherapy) increased the short-term efficacy of treatment (relative risk [RR] = 1.183, 95% confidence interval [CI] = 1.043–1.343, ) and improved patients’ quality of life (RR = 1.514, 95%CI = 1.211–1.891, ) compared with chemotherapy alone. With regard to the adverse effects, the combined treatment markedly reduced the incidence of white blood cell (WBC) reduction (RR = 0.846, 95%CI = 0.760–0.941, ), platelet reduction (RR = 0.462, 95% CI = 0.330–0.649, ), and hemoglobin reduction (RR = 0.462, 95% CI = 0.330–0.649, ) and alleviated drug-induced liver injury (RR = 0.677, 95%CI = 0.463–0.990, ). However, it did not offer a significant protective effect (RR = 0.725, 95%CI = 0.358–1.468, ). The effect of the combined treatment on the occurrence of vomiting was considerable (RR = 0.889, 95%CI = 0.794–0.996, ), and the combined treatment markedly increased the immunity of patients with lung cancer. Conclusion. The combined treatment of Shenmai injection plus chemotherapy enhanced the short-term efficacy of chemotherapy, improved the patient quality of life, alleviated the adverse effects of chemotherapeutics, and increased the patient immunity. These results should be confirmed by large-scale, high-quality RCTs.

[This corrects the article DOI: 10.1155/2018/6209679.].