Results 211 to 220 of about 2,208,935 (290)

Nail Disorders in Children With Down Syndrome: A Multicenter Study. [PDF]

open access: yesPediatr Dermatol
Sarikaya Solak S   +19 more
europepmc   +1 more source

Renal Tubular Epithelial CRLF1 Interacts With ITGB1 to Accelerate Fibrosis During the Transition From AKI to CKD

open access: yesAdvanced Science, EarlyView.
During renal fibrosis, SMAD3 acts as a transcription factor for CRLF1, promoting its expression and secretion. CRLF1 then binds to ITGB1 via an autocrine mechanism, activating the PI3K‐AKT signaling pathway to mediate renal fibrosis. This accelerates the progression from AKI to CKD, highlighting the therapeutic potential of targeting CRLF1 for ...
Chunjie Wang   +8 more
wiley   +1 more source

Crosstalk Between CTSB+ Glioblastoma Cells and S100A10+ Macrophages: A Self‐Reinforcing Circuit Promotes Immune Evasion and Limits Response to Immunotherapy

open access: yesAdvanced Science, EarlyView.
In glioblastoma, M2‐polarized macrophages secrete IL‐6, which activates STAT3 signaling in tumor cells to upregulate CTSB. Tumor‐derived CTSB binds the C‐terminus of macrophage S100A10, reinforcing M2 polarization and further IL‐6 secretion, thereby establishing a feedforward IL‐6/STAT3/CTSB/S100A10 loop. This cascade drives tumor growth, invasion, and
Hao Zhang   +11 more
wiley   +1 more source

Synergistic p53 Pathway Activation Through Sono‐Gene Therapy Induced by Ultrasound‐Triggered Theranostic Mesoporous Nanoparticles

open access: yesAdvanced Science, EarlyView.
Schematic representation of ultrasound‐mediated ICG/siCD24@MSN‐LCD from nanostructure to synergistic sono‐gene therapy. This nanoplatform targets ASGPR via the LCD shell, which dissociates to release loaded ICG and siCD24. The core mechanism involves ultrasound‐guided sonodynamic therapy by ICG and CD24 knockdown by siCD24, both activating the p53 axis
Yading Zhao   +11 more
wiley   +1 more source

Fibrillarin Resists Cellular Senescence Via SIRT1‐Dependent Nicotinamide Metabolism and Its Inhibition Sensitizes Senolytic Therapy in Esophageal Squamous Cell Carcinoma

open access: yesAdvanced Science, EarlyView.
FBL directly binds to and stabilizes SIRT1 by blocking its ubiquitin‐proteasome degradation, thereby sustaining nicotinamide metabolism and redox homeostasis to counteract cellular senescence in ESCC. Genetic and pharmacological suppression of FBL sensitizes tumor cells to senolytic therapy.
Xing Jin   +9 more
wiley   +1 more source

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