Atherogenesis, the formation of atherosclerotic plaques, is a complex process that involves several mechanisms, including endothelial dysfunction, neovascularization, vascular proliferation, apoptosis, matrix degradation, inflammation, and thrombosis. The pathogenesis and progression of atherosclerosis are explained differently by different scholars. One of the most common theories is the destruction of well-balanced homeostatic mechanisms, which incurs the oxidative stress. And oxidative stress is widely regarded as the redox status realized when an imbalance exists between antioxidant capability and activity species including reactive oxygen (ROS), nitrogen (RNS) and halogen species, non-radical as well as free radical species. This occurrence results in cell injury due to direct oxidation of cellular protein, lipid, and DNA or via cell death signaling pathways responsible for accelerating atherogenesis. This paper discusses inflammation, mitochondria, autophagy, apoptosis, and epigenetics as they induce oxidative stress in atherosclerosis, as well as various treatments for antioxidative stress that may prevent atherosclerosis.

The transformation of colloidal semiconductor magic-size clusters (MSCs) from zinc to cadmium chalcogenide (ZnE to CdE) at low temperatures has received scant attention. Here, we report the first room-temperature evolution of CdE MSCs from ZnE samples and our interpretation of the transformation pathway. We show that when prenucleation stage samples of ZnE are mixed with cadmium oleate (Cd­(OA)2), CdE MSCs evolve; without this mixing, ZnE MSCs develop. When ZnE MSCs and Cd­(OA)2 are mixed, CdE MSCs also form. We propose that Cd­(OA)2 reacts with the precursor compounds (PCs) of the ZnE MSCs but not directly with the ZnE MSCs. The cation exchange reaction transforms the ZnE PCs into CdE PCs, from which CdE MSCs develop. Our findings suggest that in reactions that lead to the production of binary ME quantum dots, the E precursor dominates the formation of binary ME PCs (M = Zn or Cd) to have similar stoichiometry. The present study provides a much more profound view of the formation and transformation mechanisms of the ME PCs.

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Survival of KRAS mutant pancreatic cancer is critically dependent on reprogrammed metabolism including elevated macropinocytosis, autophagy, and lysosomal degradation of proteins. Lysosomal acidification is indispensable to protein catabolism, which makes it an exploitable metabolic target for KRAS mutant pancreatic cancer. Herein we investigated ultra-pH-sensitive micelles (UPSM) with pH-specific buffering of organelle pH and rapid drug release as a promising therapy against pancreatic cancer. UPSM undergo micelle–unimer phase transition at their apparent pK a, with dramatically increased buffer capacity in a narrow pH range (<0.3 pH). Cell studies including amino acid profiling showed that UPSM inhibited lysosomal catabolism more efficiently than conventional lysosomotropic agents (e.g., chloroquine) and induced cell apoptosis under starved condition. Moreover, pH-triggered rapid drug release from triptolide prodrug-loaded UPSM (T-UPSM) significantly enhanced cytotoxicity over non-pH-sensitive micelles (T-NPSM). Importantly, T-UPSM demonstrated superior safety and antitumor efficacy over triptolide and T-NPSM in KRAS mutant pancreatic cancer mouse models. Our findings suggest that the ultra-pH-sensitive nanoparticles are a promising therapeutic platform to treat KRAS mutant pancreatic cancer through simultaneous lysosomal pH buffering and rapid drug release.

We report the first example of 2D covalent organic framework nanosheets (Redox‐COF1) for the selective reduction and in situ loading of valence‐variable, redox‐sensitive and long‐lived radionuclides (abbreviated as VRL nuclides). Compared with sorbents based on chemical adsorption and physical adsorption, the redox adsorption mechanism of Redox‐COF1 can effectively reduce the impact of functional group protonation under the usual high‐acidity conditions in chemisorption, and raise the adsorption efficiency from the monotonous capture by pores in physisorption. The adsorption selectivity for UO22+ reaches up to unprecedented ca. 97 % at pH 3, more than for any analogous adsorbing material.