Publications by authors named "KeKao Long"
Article Synopsis
- - Myocardial infarction (MI) is a major global health issue with high mortality, despite existing therapies, highlighting the need for new treatment strategies.
- - Exosomes, small vesicles released by various cells, show promise in promoting heart recovery by improving functions like fibrosis reduction and inflammation control, but their role in cardiac energy metabolism is still not well understood.
- - The review discusses the potential of exosome research to enhance treatments for MI, emphasizing the need for better understanding of how they affect cellular energy processes and identifying challenges for clinical application.
Article Synopsis
- M1 macrophages help protect against infections but can also contribute to diseases related to metabolism and inflammation, driven by the E3 ubiquitin ligase MDM2.
- MDM2 enhances the production of inflammatory molecules like IL-1β, MCP-1, and nitric oxide (NO) in M1 macrophages by degrading SPSB2, which stabilizes iNOS and activates the HIF-1α pathway.
- Deleting MDM2 in immune cells reduces inflammation and damage in obesity and sepsis models, but may lead to higher mortality and bacterial infections when M1 macrophage responses are suppressed.
The health concerns of microplastics (MPs) and nanoplastics (NPs) surge, but the key indicators to evaluate the adverse risks of MPs/NPs are elusive. Recently, MPs/Ps were found to disturb glucose and lipid metabolism in rodents, suggesting that MPs/NPs may play a role in obesity progression. In this study, we firstly demonstrated that the distribution of fluorescent polystyrene nanoplastics (nPS, 60 nm) white adipose tissue (WAT) of mice.
View Article and Find Full Text PDFDysfunctional triglyceride-very low-density lipoprotein (TG-VLDL) metabolism is linked to metabolic-associated fatty liver disease (MAFLD); however, the underlying cause remains unclear. The study shows that hepatic E3 ubiquitin ligase murine double minute 2 (MDM2) controls MAFLD by blocking TG-VLDL secretion. A remarkable upregulation of MDM2 is observed in the livers of human and mouse models with different levels of severity of MAFLD.
View Article and Find Full Text PDFAlthough mitophagy is known to restrict NLRP3 inflammasome activation, the underlying regulatory mechanism remains poorly characterized. Here we describe a type of early endosome-dependent mitophagy that limits NLRP3 inflammasome activation. Deletion of the endosomal adaptor protein APPL1 impairs mitophagy, leading to accumulation of damaged mitochondria producing reactive oxygen species (ROS) and oxidized cytosolic mitochondrial DNA, which in turn trigger NLRP3 inflammasome overactivation in macrophages.
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