Results 261 to 270 of about 451,629 (401)

p16Ink4a‐Positive Hepatocytes Drive Liver Fibrosis Through Activation of LIFR Family Pathway

open access: yesAdvanced Science, EarlyView.
This study found that, following the long‐term CCl4 treatment, p16high hepatocytes appeared in zone 3, spatially co‐localizing with fibrotic areas. A specific cluster of p16high hepatocytes upregulated CTF1/LIF expression which induced HSC activation and further liver fibrosis, as revealed by single cell transcriptomic analysis.
Koji Nishikawa   +23 more
wiley   +1 more source

Targeting Itga8 Mitigates Neurogenic Bladder Fibrosis Driven by Trem2⁺ Macrophage‐Derived Fn1 via FAK/RhoA/ROCK Signaling

open access: yesAdvanced Science, EarlyView.
Normal bladders exhibit quiescent fibroblasts/macrophages, whereas neurogenic bladders show acute‐phase Itga8⁺ fibroblast expansion driven by Trem2⁺ macrophage‐secreted Fn1, which activates FAK/RhoA/ROCK signaling, promotes cytoskeletal remodeling, and upregulates pro‐fibrotic genes.
Jiaxin Wang   +9 more
wiley   +1 more source

Type I Interferon Pathway Activation Disrupts Monocyte Maturation and Enhances Immune Evasion in Multiple Myeloma

open access: yesAdvanced Science, EarlyView.
This study shows that monocytes in multiple myeloma display an excessive interferon response, leading to transcriptional reprogramming and altered differentiation. Using single‐cell sequencing, coculture experiments, and patient samples before and after therapy, the authors demonstrate that induction treatment reduces this interferon response ...
Jian Cui   +18 more
wiley   +1 more source

The Disordered Region of ASXL1 Acts as an Auto‐Regulator Through Condensation

open access: yesAdvanced Science, EarlyView.
ASXL1's long IDR encodes an electrostatic “basic platform + acidic brake” that autoregulates condensation. Truncation at a clinical hotspot lifts this brake, forming condensates that retarget BRD2, remodel local chromatin accessibility, and impair neutrophil maturation.
Xiao Fang, Qiwei Li, Wenqing Zhang
wiley   +1 more source

Nuclear Factor I‐B Delays Liver Fibrosis by Inhibiting Chemokine Ligand 5 Transcription

open access: yesAdvanced Science, EarlyView.
This study identifies the transcription factor Nuclear Factor I‐B (NFIB) as a key suppressor of liver fibrosis. NFIB expression declines during hepatic stellate cell activation, and its overexpression reduces fibrosis in mice models. The mechanism involves NFIB directly repressing chemokine C─C motif ligand 5 (CCL5), thereby alleviating oxidative ...
Qianqian Chen   +14 more
wiley   +1 more source

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