Results 191 to 200 of about 9,325,572 (289)
Under pathological stimulation, NCOA4 in macrophages interacts with STAT1 to promote CH25H transcription. The subsequent increase in 25‐HC production activates macrophages, triggers inflammatory responses and ferroptosis, and accelerates the progression of AAA.
Zhinan Wu +9 more
wiley +1 more source
Microglial PBRM1 deficiency drives excessive hippocampal neurogenesis by enhancing CCL5–CCR1/5 signaling, leading to autism‐like behaviors. A pro‐inflammatory IL1α+/TNFα+ microglial subset is identified as a key cellular contributor to this process. PBRM1 represses Ccl5 expression at the transcriptional level.
Yang‐Yang Duan +12 more
wiley +1 more source
Synovial macrophages in osteoarthritis upregulate LSP1, which directly binds and inhibits SOD1, triggering a redox imbalance that activates both NOX and mitochondrial ROS pathways. This cascade drives the release of macrophage extracellular traps (METs), causing chondrocyte damage and disease progression.
Yankai Pan +9 more
wiley +1 more source
This study identifies GAP2, a bioactive polysaccharide fraction derived from Ganoderma applanatum, as a postbiotic inducer that repairs intestinal barrier damage in a gut microbiota‐dependent manner. GAP2 enriches Phocaeicola vulgatus, which degrades GAP2 and promotes tridecylic acid production, triggering Rho/CDC42 signaling and tight‐junction ...
Chuan Zhang +10 more
wiley +1 more source
Re‐Thinking Electronic Circuit Design Through Emerging Reconfigurable Field Effect Transistors
Graphical illustration of reconfigurable field effect transistor (RFET) operation modes, including n‐type, p‐type, and ambipolar transport, as well as their areas of application discussed in this review: digital circuit design, analog circuit design, post‐Shannon computing, and sensing. ABSTRACT Reconfigurable field‐effect transistors, short RFETs, are
Jens Trommer +19 more
wiley +1 more source
In this study, we demonstrate that aberrant MEKK3 signaling in endothelial cells and microglia drives the progression of cerebral cavernous malformations (CCMs). Furthermore, we identify DPDH as a potent small‐molecule MEKK3 inhibitor with substantial therapeutic potential for CCM treatment.
Weiwei Zheng +17 more
wiley +1 more source
This study reveals that age‐related LMNB1 deficiency in mesenchymal stem cells epigenetically upregulates SLC7A11, triggering actin disulfidptosis and mitochondrial dysfunction. This cascade impairs bone formation in senile osteoporosis. Furthermore, researchers identified the FDA‐approved drug naldemedine as a targeted SLC7A11 inhibitor to reverse ...
Wenhui Yu +12 more
wiley +1 more source
Meningeal Lymphatic LTBR Deficiency Links Spinal Cord Injury to Secondary Brain Pathology
Spinal cord injury (SCI) induces remote brain alterations beyond the injured spinal cord. This study links dysfunction of meningeal lymphatic vessels (mLVs) to neuroinflammation and neuronal injury after SCI. LTBR‐mediated lymphatic restoration improves meningeal lymphatic integrity and neurological outcomes, highlighting LTBR as a potential regulator ...
Yi Chen +12 more
wiley +1 more source
Combined inhibition of the WDR5 WIN pocket and HDAC activity converts SAHA‐induced hyperacetylation into a promoter state with reduced WDR5–COMPASS association and H3K4me3. MYC/E2F‐linked nascent transcription and biosynthetic recovery are suppressed, while apoptosis and senescence‐like features increase, resulting in sustained growth inhibition in ...
Jintian Song +8 more
wiley +1 more source
Thioredoxin‐2 Alleviates Osteoporosis by Restraining FOXO3a Nuclear Translocation
Endothelial TRX2 preserves bone homeostasis by retaining FOXO3a at mitochondria and limiting TRAIL production. Loss of TRX2 or oxidative stress releases FOXO3a for nuclear translocation, increasing endothelial TRAIL secretion and driving osteoclast formation and bone loss.
Chi Zhan +10 more
wiley +1 more source

