The endoplasmic reticulum (ER) is an important organelle that regulates several fundamental cellular processes, and ER dysfunction has implications for many intracellular events. The nucleotide-binding oligomerization domain-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome is an intracellularly produced macromolecular complex that can trigger pyroptosis and inflammation, and its activation is induced by a variety of signals. ER stress has been found to affect NLRP3 inflammasome activation through multiple effects including the unfolded protein response (UPR), calcium or lipid metabolism, and reactive oxygen species (ROS) generation. Intriguingly, the role of ER stress in inflammasome activation has not attracted a great deal of attention. In addition, increasing evidence highlights that both ER stress and NLRP3 inflammasome activation contribute to atherosclerosis (AS). AS is a common cardiovascular disease with complex pathogenesis, and the precise mechanisms behind its pathogenesis remain to be determined. Both ER stress and the NLRP3 inflammasome have emerged as critical individual contributors of AS, and owing to the multiple associations between these two events, we speculate that they contribute to the mechanisms of pathogenesis in AS. In this review, we aim to summarize the molecular mechanisms of ER stress, NLRP3 inflammasome activation, and the cross talk between these two pathways in AS in the hopes of providing new pharmacological targets for AS treatment.

Cardiac progenitor cells are considered to be one of the most promising stem cells for heart regeneration and repair. The cardiac protective effect of CPCs is mainly achieved by reducing tissue damage and/or promoting tissue repair through a paracrine mechanism. Exosome is a factor that plays a major role in the paracrine effect of CPCs. By delivering microRNAs to target cells and regulating their functions, exosomes have shown significant beneficial effects in slowing down cardiac injury and promoting cardiac repair. Among them, miRNA‐210 is an important anoxic‐related miRNA derived from CPCs exosomes, which has great cardiac protective effect of inhibiting myocardial cell apoptosis, promoting angiogenesis and improving cardiac function. In addition, circulating miR‐210 may be a useful biomarker for the prediction or diagnosis of related cardiovascular diseases. In this review, we briefly reviewed the mechanism of miR‐210 derived from CPCs exosomes in cardiac protection in recent years.

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Inadequate fixed carbon conversion is the main culprit for low efficiency of solid fuel chemical looping combustion (CLC). To improve the efficiency, we report here a strategy to sufficiently converse fixed carbon during corn-stalk CLC by introducing tert-butanol solution to generate adequate oxidants (H2O and CO) in cascade reaction systems. The tert-butanol solution CLC was performed at the first reaction stage using Fe2O3/Al2O3 as the oxygen carrier (OC). Then, the products of the first reaction stage act as oxidizer to drive the gasification and combustion of corn stalk in the following reaction stage at 850 °C under different peroxidation coefficients (Ω), which is a proportional coefficient of the actual amount of Fe2O3/Al2O3 used in the reaction to the theoretically calculated amount required for complete oxidation of fuel. We demonstrated that the tert-butanol solution can directly promote the gasification of corn stalk and tune the oxidation state of the reduced OC for oxidizing the fuel gas during the CLC process, which not only transfers oxygen but catalyzes corn-stalk gasification. Reaction stoichiometry and thermodynamics analysis further implied that the reported tert-butanol solutioncorn-stalk cascaded CLC is thermodynamically feasible. Organic waste solution, biomass CLC, serves the dual purpose of organic waste treatment and solid CLC promotion.

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