Ultrasound-Driven Selenium Nanoparticles Realize Bone Defect Repair through Activating Selenoproteins to Regulate PI3K/AKT Signaling Pathway DOI
Yu‐Fan Chen, Renhao Xu, Bin Xie

et al.

ACS Nano, Journal Year: 2025, Volume and Issue: unknown

Published: May 8, 2025

Excessive and variable inflammation in bone defects is a key factor that impedes effective repair. Herein, an ultrasound-controlled composite hydrogel (LNT-SeNPs@Gel) integrating gelatin-methacryloyl lentinan-decorated selenium nanoparticles (LNT-SeNPs) developed, exhibiting strong antioxidant anti-inflammatory properties to remodel the inflammatory microenvironment of defects. This serves as platform for bifunctional ultrasound (ultrasound modulation, USc repairing, USr), facilitating cascade treatment reducing overall period. During phase repair, remotely modulates LNT-SeNPs@Gel hydrogel, regulating release LNT-SeNPs inhibit overproduction reactive oxygen species (ROS) factors, ultimately remodeling microenvironment. Subsequently, USr could activate phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway regulated by selenoproteins enhance osteogenesis MC3T3-E1 cells, thereby accelerating repair process. Consequently, combination significantly improves outcomes reduces period rats. In conclusion, this study implies coordinated integration dual effects promising strategy handling complex lengthy

Language: Английский

Advances in Understanding the Pathogenesis of Sensorineural Hearing Loss: Treatment Strategies and Implications for Auditory Protection DOI Creative Commons
Lin Yan,

Yuhua Zhang,

Yongjie Wei

et al.

Published: April 20, 2025

ABSTRACT Sensorineural hearing loss (SNHL) is a prevalent multifactorial condition affecting over 1.5 billion people worldwide. Its etiology includes genetic mutations, environmental factors, and age‐related degeneration, leading to irreversible damage the cochlear hair cells auditory neurons. Although conventional interventions, such as aids implants, provide partial relief, they do not restore natural function. Recent advances in understanding of molecular mechanisms underlying SNHL, including oxidative stress, autophagy, apoptosis, ferroptosis, pyroptosis, have provided novel insights into potential therapeutic targets. Emerging treatment strategies include gene therapy, which aims correct defects through replacement editing; exosome‐based facilitates cellular repair protection; stem cell promotes neurons regeneration; nanomedicine, enables targeted drug delivery protection. Despite these promising developments, challenges remain translating therapies from preclinical research clinical applications, owing safety, efficiency, long‐term efficacy concerns. This review summarizes latest progress SNHL research, highlights key pathophysiological mechanisms, explores strategies. Understanding essential develop effective interventions prevent, potentially reverse ultimately improving quality life affected individuals.

Language: Английский

Citations

0

Ultrasound-Driven Selenium Nanoparticles Realize Bone Defect Repair through Activating Selenoproteins to Regulate PI3K/AKT Signaling Pathway DOI
Yu‐Fan Chen, Renhao Xu, Bin Xie

et al.

ACS Nano, Journal Year: 2025, Volume and Issue: unknown

Published: May 8, 2025

Excessive and variable inflammation in bone defects is a key factor that impedes effective repair. Herein, an ultrasound-controlled composite hydrogel (LNT-SeNPs@Gel) integrating gelatin-methacryloyl lentinan-decorated selenium nanoparticles (LNT-SeNPs) developed, exhibiting strong antioxidant anti-inflammatory properties to remodel the inflammatory microenvironment of defects. This serves as platform for bifunctional ultrasound (ultrasound modulation, USc repairing, USr), facilitating cascade treatment reducing overall period. During phase repair, remotely modulates LNT-SeNPs@Gel hydrogel, regulating release LNT-SeNPs inhibit overproduction reactive oxygen species (ROS) factors, ultimately remodeling microenvironment. Subsequently, USr could activate phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) signaling pathway regulated by selenoproteins enhance osteogenesis MC3T3-E1 cells, thereby accelerating repair process. Consequently, combination significantly improves outcomes reduces period rats. In conclusion, this study implies coordinated integration dual effects promising strategy handling complex lengthy

Language: Английский

Citations

0