Results 101 to 110 of about 584 (208)
Chronic rejection of transplanted organs remains an unresolved issue in clinical organ transplantation. The macrophages play a crucial role in the development of chronic rejection.
Wei Chen+4 more
doaj
Research Progress on Biomaterials with Immunomodulatory Effects in Bone Regeneration
This review highlights recent advanced in immunomodulatory biomaterials for bone repair, focusing on design strategies, immune interactions, and clinical potential. Abstract The immune system plays a pivotal role in bone regeneration, and biomaterials engineered to modulate immune responses present a promising strategy for the treatment of extensive ...
Jianan Li+11 more
wiley +1 more source
This study uncovers STAT6‐driven pulmonary fibrosis (PF) via suppression of PRKN‐mediated airway epithelial mitophagy, triggering mitochondrial dysfunction and ferroptosis. Rifabutin is identified as a potent STAT6 inhibitor that effectively reverses fibrotic progression. These findings reveal the STAT6‐PRKN axis as a pathogenic regulator and provide a
Youjing Yang+7 more
wiley +1 more source
TFEB drives mTORC1 hyperactivation and kidney disease in Tuberous Sclerosis Complex
Tuberous Sclerosis Complex (TSC) is caused by TSC1 or TSC2 mutations, leading to hyperactivation of mechanistic target of rapamycin complex 1 (mTORC1) and lesions in multiple organs including lung (lymphangioleiomyomatosis) and kidney (angiomyolipoma ...
Nicola Alesi+20 more
doaj +1 more source
This study reveals that the glycolytic enzyme HK2 mediates hypoxia‐induced astrocytic exosome biogenesis by directly phosphorylating nSMase1. These astrocytic exosomes impair brain endothelial tight junctions. Astrocyte‐specific knockdown of HK2 reduces exosome release and alleviates brain injury after MCAO.
Chen Chen+12 more
wiley +1 more source
This study highlights GRK2 is a central mediator in OSS‐induced endothelial dysfunction. OSS activates GPCRs in endothelial cells, leading to GRK2 phosphorylation and the activation of AP‐1. AP‐1 induces inflammation, while also promoting NR4A1 expression and anchoring LKB1 in the nucleus, which suppresses AMPK activity. This cascade causes endothelial
Li‐Da Wu+18 more
wiley +1 more source
ATF3 Deficiency Exacerbates Ageing‐Induced Atherosclerosis and Clinical Intervention Strategy
Targeting ATF3 with terazosin to against VSMC Senescence and atherosclerosis. TZ reduces the binding affinity of YTHDF2 to Atf3 mRNA, while enhancing mRNA stability. ATF3 promotes Atg7 transcription, enhancing autophagy. ATG7 binds to ATF3 in the cytoplasm, facilitating ATF3 translocation to the nucleus and establishing positive feedback. By modulating
Hao Nie+11 more
wiley +1 more source
Gasdermin D (GSDMD) does not only reduce pancreatic enzyme synthesis but also induces pancreatic acinar cells to express mucin 1 (MUC1), which forms a barrier to prevent digestive enzyme‐mediated digestion. However, GSDMD can promote the secretion of inflammatory cytokines by macrophages and aggravate pancreatic histological injury by expanding ...
Chaoxu Liu+10 more
wiley +1 more source
Epigenetic Regulation of DAPK1 and Netrin‐1 Drives Diabetic Encephalopathy
This study identifies a microRNA (miR)‐216a‐5p/death‐associated protein kinase 1 (DAPK1)/hepatocyte nuclear factor 1 homeobox A (HNF1A)/Netrin‐1 signaling axis in diabetic encephalopathy (DE). In leptin receptor‐deficient (db/db) and streptozotocin (STZ)‐induced diabetic mice, reduced miR‐216a‐5p increases DAPK1 expression, disrupting HNF1A binding to ...
Yang Zhou+13 more
wiley +1 more source