Atrazine (ATR) is a widely used herbicide worldwide that can cause kidney damage in humans and animals by accumulation in water and soil. Lycopene (LYC), a carotenoid with numerous biological activities, plays an important role in kidney protection due to its potent antioxidant and anti-inflammatory effects. The current study sought to investigate the role of interactions between mtDNA and the cGAS-STING signaling pathway in LYC mitigating PANoptosis and inflammation in kidneys induced by ATR exposure. In our research, 350 mice were orally administered LYC (5 mg/kg BW/day) and ATR (50 or 200 mg/kg BW/day) for 21 days. Our results reveal that ATR exposure induces a decrease in mtDNA stability, resulting in the release of mtDNA into the cytoplasm through the mPTP pore and the BAX pore and the mobilization of the cGAS-STING pathway, thereby inducing renal PANoptosis and inflammation. LYC can inhibit the above changes caused by ATR. In conclusion, LYC inhibited ATR exposure-induced histopathological changes, renal PANoptosis, and inflammation by inhibiting the cGAS-STING pathway. Our results demonstrate the positive role of LYC in ATR-induced renal injury and provide a new therapeutic target for treating renal diseases in the clinic.
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http://dx.doi.org/10.1021/acs.jafc.4c02820 | DOI Listing |
Neuromolecular Med
December 2024
Department of Neurology, Liaocheng People's Hospital and Liaocheng Hospital Affiliated to Shandong First Medical University, Liaocheng, 252000, China.
Alzheimer's disease (AD) is a common progressive neurodegenerative disorder, and the vast majority of cases occur in elderly patients. Recently, the accumulation of Aβ and tau proteins has drawn considerable attention in AD research. This review explores the multifaceted interactions between these proteins and their contribution to the pathological landscape of AD, encompassing synaptic dysfunction, neuroinflammation, and PANoptosis.
View Article and Find Full Text PDFTrends Biotechnol
December 2024
Department of General Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an 710061, China. Electronic address:
Inflammatory bowel disease (IBD) is a chronic relapsing immune-mediated inflammatory disorder of the alimentary tract without exact etiology. Mitochondrial reactive oxygen species (mtROS) derived from mitochondrial dysfunction impair intestinal barrier function, increase gut permeability, and facilitate immune cell invasion, and, therefore, are considered to have a pivotal role in the pathogenesis of IBD. Here, we reprogrammed regulatory T cell (Treg)-derived exosomes loaded with the antioxidant trace element selenium (Se) and decorated them with the synthetic mitochondria-targeting SS-31 tetrapeptide via a peptide linker.
View Article and Find Full Text PDFBiomaterials
May 2025
Department of Orthopedic Surgery, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, 600 Yishan Road, Shanghai, 200233, China. Electronic address:
Necrosis at the distal end of random skin flaps remains a significant challenge, limiting the clinical application of these flaps in plastic and reconstructive surgery. Inhibiting ischemia/reperfusion (I/R) injury and promoting the formation of neovascular networks are critical preventive strategies. Platelet-derived small extracellular vesicles (PL-sEV) are nanocarriers of growth factors that provide an alternative to clinically used platelet-rich plasma and platelet lysates, offering higher growth factor concentrations and lower immunogenicity.
View Article and Find Full Text PDFJ Inflamm Res
December 2024
Pulmonary and Critical Care Medicine, China Aerospace Science & Industry Corporation 731 hospital, Beijing, 100074, People's Republic of China.
Pharmacol Res
December 2024
Center for Drug Research and Development, Guangdong Pharmaceutical University, Guangzhou 510006, China; Key specialty of Clinical Pharmacy, The first Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou 510699, China. Electronic address:
Ulcerative colitis (UC) is characterized by increased cell death in intestinal epithelial cell (IEC), which compromises gut barrier function and activates inflammation. Aberrant mitochondrial dynamics have been implicated in various forms of cell death, but it is currently unclear if they play a role in IEC death and colitis pathogenesis. This study aims to investigate the contribution of aberrant mitochondrial dynamics to colitis progression using cellular models, animal models, and clinical samples.
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