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Global warming and the energy shortage due to the burning of fossil fuels are two major challenges. A strategy of light‐driven catalytic dry reforming of methane (DRM) using inexhaustible solar energy has provided an effective approach to tackle these challenges. Loaded metallic Ni nanoparticles have been identified as promising catalysts as alternatives to noble metals for DRM. However, they suffer from quick deactivation caused by severe coking due to thermodynamically inevitable side‐reactions. Herein, a unique nickel half‐metal catalyst of monolayer nickel clusters stabilized by alumina is reported, with 100% atomic utilization efficiency and extraordinary catalytic performance for light‐driven DRM, dramatically different from its counterpart of conventional metallic Ni nanoparticles. It has extremely high specific H2 and CO production rates of 8572.96 and 9614.26 mmol min−1 gNi−1, more than one order of magnitude higher than those of Ni nanoparticles. No detectable coke is formed due to the alteration of kinetic processes for DRM, resulting in the inhibition of coke deposition. It is discovered that light not only significantly enhances catalytic activity, but also enables quick thermocatalytic deactivation to be durable due to the oxidation of carbon species and the desorption of strongly adsorbed CO2 and CO being dramatically promoted by light. [ABSTRACT FROM AUTHOR]

Normal heart development is vital for maintaining its function, and the development process is involved in complex interactions between different cell lineages. How mammalian hearts develop differently is still not fully understood. In this study, we identified several major types of cardiac cells, including cardiomyocytes (CMs), fibroblasts (FBs), endothelial cells (ECs), ECs/FBs, epicardial cells (EPs), and immune cells (macrophage/monocyte cluster, MACs/MONOs), based on single-cell transcriptome data from embryonic hearts of both human and mouse. Then, species-shared and species-specific marker genes were determined in the same cell type between the two species, and the genes with consistent and different expression patterns were also selected by constructing the developmental trajectories. Through a comparison of the development stage similarity of CMs, FBs, and ECs/FBs between humans and mice, it is revealed that CMs at e9.5 and e10.5 of mice are most similar to those of humans at 7 W and 9 W, respectively. Mouse FBs at e10.5, e13.5, and e14.5 are correspondingly more like the same human cells at 6, 7, and 9 W. Moreover, the e9.5-ECs/FBs of mice are most similar to that of humans at 10W. These results provide a resource for understudying cardiac cell types and the crucial markers able to trace developmental trajectories among the species, which is beneficial for finding suitable mouse models to detect human cardiac physiology and related diseases. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the protective effect of curcumin (Cu) on myocardial injury in diabetic cardiomyopathy in vivo and in vitro. Serum and myocardial glucose, inflammatory cytokines, and cardiac function indexes of type 2 diabetes db/db mice were measured. The mechanism of action was confirmed by immunohistochemistry, immunofluorescence, and western blot experiments. H9C2 cells stimulated by glucose (Glu) were used as cell models in vitro. Cu treatment improved glucose tolerance and lipid profile and reduced the production of inflammatory cytokines. In addition, Cu decreased the serum biochemical indexes. Cu inhibits high mobility group box 1 (HMGB1) signaling pathway in db/db mice. Cu treatment also significantly inhibited pa‐induced inflammatory signaling pathway in H9C2 cells. HMGB1 inhibitor or HMGB1 knockdown counteracted the effects of Cu on diabetic cardiomyopathy. The present study showed the protective effects of Cu on myocardial injury via HMGB1 pathway in diabetic cardiomyopathy in vivo and in vitro. [ABSTRACT FROM AUTHOR]

Background/Aims: Cardiac fibrosis after myocardial infarction (MI) has been identified as a key factor in the development of heart failure, but the mechanisms undelying cardiac fibrosis remained unknown. microRNAs (miRNAs) are novel mechanisms leading to fibrotic diseases, including cardiac fibrosis. Previous studies revealed that miR-22 might be a potential target. However, the roles and mechanisms of miR-22 in cardiac fibrosis remained ill defined. The present study thus addressed the impact of miR-22 in cardiac fibrosis. Methods: After seven days following coronary artery occlusion in mice, tissues used for histology were collected and processed for Masson's Trichrome staining. In addition, cardiac fibroblasts were transfected with mimics and inhibitors of miR-22 using Lipofectamin 2000, and luciferase activity was measured in cell lysates using a luciferase assay kit. Western blotting was used to detect the expression of collagen1, α-SMA and TGFβRI proteins levels, and real time-PCR was employed to measure the Col1α1, Col3α1, miR-22 and TGFβRI mRNA levels. Results: In this study, we found that miR-22 was dynamically downregulated following MI induced by permanent ligation of the left anterior descending coronary artery for 7 days, an effect paralleled by significant collagen deposition. Inhibition of miR-22 with AMO-22 resulted in increased expression of Col1α1, Col3α1 and fibrogenesis in cultured cardiac fibroblasts. Conversely, overexpression of miR-22 in cultured cardiac fibroblasts significantly abrogated angiotensin II-induced collagen formation and fibrogenesis. Furthermore, we found that TGFβRI is a direct target for miR-22, and downregulation of TGFβR may have mediated the antifibrotic effect of miR-22. Conclusion: Our data clearly demonstrate that miR-22 acts as a novel negative regulator of angiotensin II-induced cardiac fibrosis by suppressing the expression of TGFβRI in the heart and may represent a new potential therapeutic target for treating cardiac fibrosis. [ABSTRACT FROM AUTHOR]

Context: Ischemia/hypoxia and reperfusion impair mitochondria and produce a large amount of reactive oxygen species (ROS), which lead to mitochondrial and brain damage. Furthermore, heme oxygenase-1 (HO-1) as a cytoprotective gene protects cells against ROS-induced cell death in ischemia–reperfusion injury. Induction of HO-1 is involved in cytoprotective effects of taxol. Objective: We hypothesize that taxol protects cardiac myocytes possibly by preserving myocardial mitochondrial function and inducing HO-1 expression through the JNK pathway. Materials and methods: In this project, the perfused Langendorff hearts isolated from rats were randomly divided into five groups: control, ischemic, ischemic + taxol (0.1 μM), ischemic + taxol (0.3 μM), and ischemic + taxol (1 μM). Briefly, following a 15 min equilibration period, the control group was subject to normoxic perfusion for 120 min; the ischemia group, normoxic reperfusion for 120 min after 30 min ischemia; the taxol groups, normoxic reperfusion for 120 min after 30-min ischemia with taxol (0.1, 0.3, or 1 μM). The microtubule disruption score, ROS levels, and the activity of mitochondrial electron transport chain complexes I and III were examined by using immunohistochemical methods and free radical detection kits. Western blot assay was employed to study the underlying mechanisms. Results: After Taxol treatment (0.1 µM), the ischemic microtubule disruption score was reduced to 9.8 ± 1.9%. The study revealed that 0.1, 0.3, and 1 μM taxol reduced the level of ROS by 33, 46 and 51%, respectively (p < 0.05). In additional, 0.3 and 1 μM taxol dramatically increased the activity of mitochondrial electron transport chain complex I (99.11 ± 2.59, 103.49 ± 3.89) and mitochondrial electron transport chain complex III (877.82 ± 12.08; 907.42 ± 16.21; 914.73 ± 19.39, *p < 0.05). Additionally, phosphorylation levels of JNK1 were significantly increased in the taxol group. Furthermore, the expression level of HO-1 increased with taxol treatments, which could be inhibited by the specific inhibitor of JNK, SP600125. Discussion and conclusion: Taxol stabilized microtubules and effectively reduced ROS levels during ischemia. It also preserved the activity of mitochondrial complexes I and III. Interestingly, taxol induced the expression of HO-1 via the JNK pathway in cardiac myocytes. [ABSTRACT FROM AUTHOR]