Supported metal nanostructures are the most widely used type of heterogeneous catalyst in industrial processes. The size of metal particles is a key factor in determining the performance of such catalysts. In particular, because low-coordinated metal atoms often function as the catalytically active sites, the specific activity per metal atom usually increases with decreasing size of the metal particles. However, the surface free energy of metals increases significantly with decreasing particle size, promoting aggregation of small clusters. Using an appropriate support material that strongly interacts with the metal species prevents this aggregation, creating stable, finely dispersed metal clusters with a high catalytic activity, an approach industry has used for a long time. Nevertheless, practical supported metal catalysts are inhomogeneous and usually consist of a mixture of sizes from nanoparticles to subnanometer clusters. Such heterogeneity not only reduces the metal atom efficiency but also frequently leads to undesired side reactions. It also makes it extremely difficult, if not impossible, to uniquely identify and control the active sites of interest.The ultimate small-size limit for metal particles is the single-atom catalyst (SAC), which contains isolated metal atoms singly dispersed on supports. SACs maximize the efficiency of metal atom use, which is particularly important for supported noble metal catalysts. Moreover, with well-defined and uniform single-atom dispersion, SACs offer great potential for achieving high activity and selectivity.In this Account, we highlight recent advances in preparation, characterization, and catalytic performance of SACs, with a focus on single atoms anchored to metal oxides, metal surfaces, and graphene. We discuss experimental and theoretical studies for a variety of reactions, including oxidation, water gas shift, and hydrogenation. We describe advances in understanding the spatial arrangements and electronic properties of single atoms, as well as their interactions with the support. Single metal atoms on support surfaces provide a unique opportunity to tune active sites and optimize the activity, selectivity, and stability of heterogeneous catalysts, offering the potential for applications in a variety of industrial chemical reactions.

Objective The role of receptors for endogenous metabolic danger signals-associated molecular patterns (DAMPs) has been characterized recently as bridging innate immune sensory systems for DAMPs to initiation of inflammation in bone marrow-derived cells such as macrophages. However, it remains unknown whether endothelial cells (ECs), the cell type with the largest numbers and the first vessel cell type exposed to circulating DAMPs in the blood, can sense hyperlipidemia. This report determined whether caspase-1 plays a role in ECs in sensing hyperlipidemia and promoting EC activation. Approach and Results Using biochemical, immunological, pathological and bone marrow transplantation methods together with the generation of new apoplipoprotein E (ApoE)−/−/caspase-1−/− double knock-out mice we made the following observations: 1) early hyperlipidemia induced caspase-1 activation in ApoE−/− mouse aorta; 2) caspase-1−/−/ApoE−/− mice attenuated early atherosclerosis; 3) caspase-1−/−/ApoE−/− mice had decreased aortic expression of pro-inflammatory cytokines and attenuated aortic monocyte recruitment; and 4) caspase-1−/−/ApoE−/− mice had decreased EC activation including reduced adhesion molecule expression and cytokine secretion. Mechanistically, oxidized lipids activated caspase-1 and promoted pyroptosis in ECs by a ROS mechanism. Caspase-1 inhibition resulted in accumulation of sirtuin 1 (Sirt1) in the ApoE−/− aorta, and Sirt1 inhibited caspase-1 upregulated genes via activator protein-1 (AP-1) pathway. Conclusions Our results demonstrate for the first time that early hyperlipidemia promotes EC activation before monocyte recruitment via a caspase-1-Sirt1-AP-1 pathway, which provides an important insight into the development of novel therapeutics for blocking caspase-1 activation as early intervention of metabolic cardiovascular diseases and inflammations.

Uric acid is the product of purine metabolism. It is known that hyperuricemia, defined as high levels of blood uric acid, is the major etiological factor of gout. A number of epidemiological reports have increasingly linked hyperuricemia with cardiovascular and neurological diseases. Studies highlighting the pathogenic mechanisms of uric acid point to an inflammatory response as the primary mechanism for inducing gout and possibly contributing to uric acid's vascular effects. Monosodium urate (MSU) crystals induce an inflammatory reaction, which are recognized by Toll-like receptors (TLRs). These TLRs then activate NALP3 inflammasome. MSU also triggers neutrophil activation and further produces immune mediators, which lead to a proinflammatory response. In addition, soluble uric acid can also mediate the generation of free radicals and function as a pro-oxidant. This review summarizes the epidemiological studies of hyperuricemia and cardiovascular disease, takes a brief look at hyperuricemia and its role in neurological diseases, and highlights the studies of the advanced pathological mechanisms of uric acid and inflammation.