Bismuth vanadate (BiVO), a well-known semiconductor photocatalyst with various advantages, has shown great potential in addressing energy and environmental issues. However, its inherent drawbacks restrict the photocatalytic performance of pure BiVO. In the past few years, many efforts have been devoted to improving the catalytic activity of BiVO and revealing the degradation mechanism in depth. In this review, we summarized the recent progress on BiVO in the field of photocatalytic degradation, including the strategies which enhance light absorption ability and suppress the recombination of charge carriers of BiVO, as well as the related degradation mechanism. Finally, future prospects and challenges are summarized, which may provide new guidelines for designing more effective BiVO-based photocatalysts for the degradation of persistent organic pollutants.
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http://dx.doi.org/10.3390/nano15050331 | DOI Listing |
Plant Physiol
March 2025
College of Life and Environmental Sciences, Hangzhou Normal University, Hangzhou, China.
Detoxifying reactive oxygen species (ROS) that accumulate under saline conditions is crucial for plant salt tolerance. The Salt Overly Sensitive (SOS) pathway functions upstream, while flavonoids act downstream, in ROS scavenging under salt stress. However, the potential crosstalk between the SOS pathway and flavonoids in regulating salt stress responses and the associated mechanisms remain largely unexplored.
View Article and Find Full Text PDFJ Immunol
January 2025
Key Laboratory of Breeding Biotechnology and Sustainable Aquaculture, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan, P. R. China.
The von Hippel-Lindau (VHL) tumor suppressor gene VHL is a classic tumor suppressor that has been identified in family members with clear cell renal cell carcinomas, central nervous system and retinal hemangioblastomas, phaeochromocytomas, and pancreatic neuroendocrine tumors. The well-defined function of VHL is to mediate proteasomal degradation of hydroxylated hypoxia-inducible factor α proteins, resulting in the downregulation of hypoxia-responsive gene expression. Previously, we reported that VHL inhibits antiviral signaling by targeting mitochondrial antiviral signaling protein (MAVS) for proteasomal degradation.
View Article and Find Full Text PDFJ Immunol
January 2025
Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA, United States.
Macrophages are critical to maintaining and restoring tissue homeostasis during inflammation. The lipid metabolic state of macrophages influences their function and polarization, which is crucial to the resolution of inflammation. The contribution of lipid synthesis to proinflammatory macrophage responses is well understood.
View Article and Find Full Text PDFJ Immunol
January 2025
Institute of Virology and Immunology, Mittelhäusern, Switzerland.
While several African swine fever virus (ASFV)-encoded proteins potently interfere with the cGAS-STING (cyclic GMP-AMP synthetase-stimulator of interferon genes) pathway at different levels to suppress interferon (IFN) type I production in infected macrophages, systemic IFN-α is induced during the early stages of AFSV infection in pigs. The present study elucidates a mechanism by which such responses can be triggered, at least in vitro. We demonstrate that infection of monocyte-derived macrophages (MDMs) by ASFV genotype 2 strains is highly efficient but immunologically silent with respect to IFN type I, IFN-stimulated gene induction, and tumor necrosis factor production.
View Article and Find Full Text PDFJ Immunol
January 2025
Institute of Microbiology and Immunology, National Yang Ming Chiao Tung University, Taipei City, Taiwan.
Decoy receptor 3 (DcR3), a soluble receptor in the tumor necrosis factor receptor superfamily, regulates the functions of monocytes, macrophages, dendritic cells, and T cells. Previous studies have demonstrated that DcR3 suppresses B cell proliferation in vitro and ameliorates autoimmune diseases in animal models; however, whether and how DcR3 regulates antibody production is unclear. Using a DcR3 transgenic mouse model, we found that DcR3 impaired the T cell-dependent antigen-stimulated antibody response.
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