Ferroptosis, an unusual nonapoptotic cell death caused by iron-dependent accumulation of lipid peroxide, enables flexible design of antitumor platform. Specifically, as a positive role, ferroptosis can induce immune response accompanied...
Since 2008, China has introduced state-led financialization to inject low-interest, stable and long-term loans to facilitate urban redevelopment through national shantytown redevelopment schemes (SRSs). Extending critical state theories to China’s transitional economy, we consider SRSs to be a policy model of the state project (mode of policy-making) of crisis management that aims to revitalize the national economy in the wake of the global financial crisis. Essentially, this state project serves to tackle the legitimation crisis threatened by both the economic crisis and the escalating social discontent. Drawing on an empirical study of Chengdu, a regional hub in western China spearheading SRSs, this paper examines how the Chinese state at different levels interacts with the nascent financial market in the creation of a new “model” of urban redevelopment under state-led financialization. Having been exploited to manage economic and legitimation crises, this model has simultaneously become a source of “crisis of crisis-management” owing to the state’s “over-intervention”. This research contributes to a fresh understanding of the multiplicity of financialization by linking the financialization of urban built environment with the financialization of the state project, in which financial motives and practices shape the mode of policy making. The Chinese experience also presents a decentered interpretation of state-led financialization that renews our understanding of the multifaceted state and state projects, particularly the hybridized, often contradictory motivations and socio-economic outcomes of state interventions.
Current programmed death‐1 ligand (PD‐L1)‐based therapy focuses on local tumors. However, circulating exosomal PD‐L1 possesses inherent anti‐PD‐L1 blockade resistance and dominates tumor metastasis, playing a critical role in systemic immunosuppression. Therefore, the efficacy of immune checkpoint therapy depends on simultaneously decreasing tumoral and circulating exosomal PD‐L1. However, such therapeutic platforms have never been reported so far. Herein, a PD‐L1 checkpoint‐regulatable immune niche created by an injectable hydrogel is reported to reprogram PD‐L1 of both tumor and circulating exosomes. Oxidized sodium alginate‐armored tumor membrane vesicle (O‐TMV) as a gelator, with Ca2+ channel inhibitor dimethyl amiloride (DMA) and cyclin‐dependent kinase 5 (Cdk5) inhibitor roscovitine formed hydrogel (O‐TMV@DR) in vivo, work as an antigen depot to create an immune niche. O‐TMV chelates Ca2+ within the tumor environment and DMA continuously prevents cellular Ca2+ influx, suppressing Ca2+‐governed exosome secretion with decreased exosome number. Roscovitine not only down‐regulates tumor cell PD‐L1 expression along with decreasing exosomal PD‐L1 expression inherited from parental tumor cells via a genetic blockade effect, but also blunts the cascade connection between PD‐L1 up‐regulation and interferon‐γ stimulation, achieving down‐regulated PD‐L1 expression in both tumor cells and exosomes. Therefore, a full‐scale reprogramming of both tumoral PD‐L1 and exosomal PD‐L1 is achieved, offering an innovative immune checkpoint‐regulatable cancer immunotherapy
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