Results 231 to 240 of about 814,199 (330)

Hepatocyte‐Derived Extracellular Vesicles Deliver miR‐328‐3p to Trigger PP2A‐B56δ–Mediated p‐NLRP3S295‐Dependent Metaflammation in Macrophages upon Microcystin‐LR Exposure

open access: yesAdvanced Science, EarlyView.
Hepatocyte‐derived extracellular vesicles deliver miR‐328‐3p to trigger PP2A‐B56δ–mediated p‐NLRP3S295‐dependent metaflammation in macrophages upon microcystin‐LR exposure. 2‐DG, 2‐deoxy‐D‐glucose. B56δ, protein phosphatase 2A‐B56δ. ER, endoplasmic reticulum. iHD‐EV, inducible hepatocyte‐derived extracellular vesicles. IP3R, inositol 1,4,5‐triphosphate
Jia‐Shen Wu   +13 more
wiley   +1 more source

Inflammatory mechanisms contribute to long-term cognitive deficits induced by perinatal asphyxia via interleukin-1. [PDF]

open access: yesNeuropsychopharmacology
Kelemen H   +21 more
europepmc   +1 more source

Platelet Rubicon Bidirectional Regulation of GPVI and Integrin αIIbβ3 Signaling Mitigates Stroke Infarction Without Compromising Hemostasis

open access: yesAdvanced Science, EarlyView.
This study identifies Rubicon as a key platelet protein that bidirectionally regulates GPVI and integrin αIIbβ3 signaling. Platelet Rubicon protects against cerebral ischemia‐reperfusion injury by limiting infarction without increasing hemorrhage.
Xiaoyan Chen   +11 more
wiley   +1 more source

Inhibition of interleukin-1 or -6 after myocardial infarction: pros, cons, and future perspectives. [PDF]

open access: yesEur Heart J Cardiovasc Pharmacother
Galli M   +3 more
europepmc   +1 more source

Ribosome Homeostasis Regulated by SETD2 Preserves Intestinal Epithelial Barrier

open access: yesAdvanced Science, EarlyView.
SETD2 ablation causes dysregulation and recruitment defects of ribosome biogenesis factors, resulting in translational disorders of barrier maintenance genes, thereby compromising the intestinal barrier. These findings unveil a previously unappreciated role of ribosome biogenesis and translational regulation in preserving the intestinal epithelial ...
Hanyu Rao   +11 more
wiley   +1 more source

Dysfunctional TRIM31 of POMC Neurons Provokes Hypothalamic Injury and Peripheral Metabolic Disorder under Long‐Term Fine Particulate Matter Exposure

open access: yesAdvanced Science, EarlyView.
Particulate matter ≤2.5 µm (PM2.5) elevates risks of neurological and chronic metabolic diseases, but the underlying mechanisms linking PM2.5‐induced central nervous system (CNS) injury to metabolic dysfunction remain unclear. Hypothalamic pro‐opiomelanocortin‐expressing (POMC+) neurons regulate systemic metabolic homeostasis, and tripartite motif ...
Chenxu Ge   +21 more
wiley   +1 more source

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