Migrasomes, a new mode of intercellular communication.

Migrasomes are newly discovered extracellular vesicles (EVs) that are formed in migrating cells and mediate intercellular communication. However, their size, biological generation, cargo packaging, transport, and effects on recipient cells by migrasomes are different from those of other EVs. In addition to mediating organ morphogenesis during zebrafish gastrulation, discarding damaged mitochondria, and lateral transport of mRNA and proteins, growing evidence has demonstrated that migrasomes mediate a variety of pathological processes. In this review, we summarize the discovery, mechanisms of formation, isolation, identification, and mediation of cellular communication in migrasomes. We discuss migrasome-mediated disease processes, such as osteoclast differentiation, proliferative vitreoretinopathy, tumor cell metastasis by PD-L1 transport, immune cell chemotaxis to the site of infection by chemokines, angiogenesis promotion via angiogenic factors by immune cells, and leukemic cells chemotaxis to the site of mesenchymal stromal cells. Moreover, as new EVs, we propose the potential of migrasomes for disease diagnosis and treatment. Video Abstract.

Helminth infection and helminth-derived products: A novel therapeutic option for non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is closely related to obesity, diabetes, and metabolic syndrome (MetS), and it has become the most common chronic liver disease. Helminths have co-evolved with humans, inducing multiple immunomodulatory mechanisms to modulate the host's immune system. By using their immunomodulatory ability, helminths and their products exhibit protection against various autoimmune and inflammatory diseases, including obesity, diabetes, and MetS, which are closely associated with NAFLD. Here, we review the pathogenesis of NAFLD from abnormal glycolipid metabolism, inflammation, and gut dysbiosis. Correspondingly, helminths and their products can treat or relieve these NAFLD-related diseases, including obesity, diabetes, and MetS, by promoting glycolipid metabolism homeostasis, regulating inflammation, and restoring the balance of gut microbiota. Considering that a large number of clinical trials have been carried out on helminths and their products for the treatment of inflammatory diseases with promising results, the treatment of NAFLD and obesity-related diseases by helminths is also a novel direction and strategy.

Assembly of polycyclic N-heterocycles via copper-catalyzed cycloamination of indolylquinones and aromatic amines.

The copper-catalyzed cycloamination of indolylquinones and various (hetero)aromatic amines under ligand-free conditions for the synthesis of polycyclic N-heterocycles has been developed. This method allows facile access to polycyclic N-heterocycles with the tolerance of chloride, bromide, amino, thio, etc. groups in moderate to high yields (60-89%).

Association between leukocyte mitochondrial DNA content and risk of coronary heart disease: a case-control study.

OBJECTIVE: Compelling epidemiological evidence indicates that alterations of mitochondrial DNA (mtDNA), including mutations and abnormal content of mtDNA, are associated with the initiation and development of cardiovascular disease. This study was undertaken to investigate whether mtDNA content in peripheral blood leukocytes (PBLs) could be used as a risk predictor for coronary heart disease (CHD). METHODS: The mtDNA content of PBLs from 378 CHD patients and 378 matched healthy controls was measured using quantitative real-time PCR-based method in a case-control study. An unconditional multivariate logistic regression model was applied to estimate the association between leukocyte mtDNA content and CHD risk. RESULTS: CHD patients exhibited notably lower mtDNA content than matched healthy controls (median, 0.65 vs. 0.86; P < 0.001). Compared with individuals who had high mtDNA content, individuals who had low mtDNA content had a significantly increased risk of CHD (adjusted OR, 2.38; 95% confidence interval, 1.33-4.69). A significant dose-response relation was observed between increased CHD risk and lower mtDNA content (Ptrend < 0.001). Furthermore, there was a significantly positive mtDNA content correlation between PBLs and atherosclerotic plaque tissue (ρ = 0.627, P = 0.039). In addition, a significant joint effect on the risk of CHD was noted between mtDNA content and cigarette smoking or plasma LDL-C concentration. CONCLUSIONS: This present study provide the first epidemiologic evidence linking low mtDNA content in PBLs to an increased CHD risk, which warrants further investigation in other populations.