Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

α7nAChR activation reduces inflammation and apoptosis, promoting muscle regeneration through the AKT-FOXO1 pathway.

ABSTRACT: Inflammatory factors can lead to muscle atrophy. Therefore, this study aims to further explore the role of inflammatory molecules in muscle atrophy and establish an in vitro inflammatory muscle atrophy model.

ORGANISM(S): Mus musculus

PROVIDER: GSE304280 | GEO | 2026/03/30

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

α7nAChR activation reduces inflammation and apoptosis, promoting muscle regeneration through the AKT-FOXO1 pathway.

Project description:α7nAChR activation reduces inflammation and apoptosis, promoting muscle regeneration through the AKT-FOXO1 pathway.

| PRJNA1299810 | ENA

Akt-mediated foxo1 inhibition is required for liver regeneration.

Project description: Not available

| S-EPMC5177729 | biostudies-literature

Microarray analysis of transgenic mice specifically overexpressing FOXO1 in skeletal muscle (FOXO1 Tg mice)

Project description:FOXO1, a member of the FOXO forkhead type transcription factors, is markedly up-regulated in skeletal muscle during atrophy. Previously, we created transgenic mice specifically overexpressing FOXO1 in skeletal muscle (FOXO1 Tg mice). These mice weighed less than the wildtype control mice, had a reduced skeletal muscle mass. In this study, to better understand changes in skeletal muscle during atrophy, we performed a microarray analysis of skeletal muscle in wild-type control and FOXO1 Tg mice. The microarray data shows that in the skeletal muscles of FOXO1 Tg mice, gene expression of PGC-1β, a transcriptional regulator whose increased expression activates energy-expenditure-related genes in skeletal muscles, is decreased.

2020-07-07 | GSE146919 | GEO

Increased global DNA methylation by Dnmt3a disrupts skeletal muscle homeostasis, promotes age-related muscle atrophy, and reduces muscle metabolic elasticity

Project description:Loss of muscle mass and function—a hallmark of skeletal muscle aging—is known as sarcopenia. Moreover, mammalian aging is reportedly driven by loss of epigenetic information. However, the effect of epigenetic alterations on skeletal muscle homeostasis is unknown. In this study, we show that chronic elevation of global DNA methylation results in a myopathy-like phenotype and age-related changes in skeletal muscle. Overexpression of muscle de novo methyltransferase 3a (Dnmt3a) increased central nucleus-positive myofibers, predominantly in fast-twitch myofibers, and shifted muscle fiber type to stress-resistant slow-twitch myofibers, accompanied by increased inflammatory and senescent signatures, decreased mitochondrial OXPHOS complex I protein level, and reduced basal autophagy in skeletal muscle. Chronic Dnmt3a overexpression decreased muscle mass and strength, and impaired tolerance to endurance exercise with age. This age-related decline in endurance exercise capacity was accompanied by an augmented inflammatory signature in a manner that is enhanced with age and promoted muscle atrophy. Network analysis identified Akt1 as a potential hub gene. Dnmt3a expression not only reduced sensitivity to starvation-induced muscle atrophy by suppressing the FoxO-regulated autophagy and ubiquitin–proteasome systems, but also reduced the restorability from starvation-induced muscle atrophy. These data suggest that increased global DNA methylation disrupts skeletal muscle homeostasis, promotes age-related muscle atrophy, and reduces muscle metabolic elasticity.

2025-01-16 | GSE262342 | GEO

Effect of depletion of FAM129B on gene expression during skeletal muscle differentiation of C2C12 cells

Project description:Muscle atrophy, a decline in muscle mass and quantity caused by a variety of factors such as cancer, aging, and long-term use of glucocorticoids, manifested at the molecular level as excessive protein catabolism. Muscle atrophy severely affects the quality of life and the treatment remains an unresolved challenge. FAM129B is an antioxidant protein that plays a key role in signal transduction.FAM129B has previously been reported to be involved in muscle growth and development in cattle. The current study aims to describe the role of FAM129B in muscle atrophy, which is expected to be a potential therapeutic target for skeletal muscle atrophy.

2025-06-01 | GSE273604 | GEO

Jakyak-gamcho-tang ameliorates dexamethasone (DEX)-induced muscle atrophy and muscle dysfunction [Gastrocnemius and Soleus]

Project description:Jakyak-gamcho-tang (JGT) is a herbal medicine that has been traditionally prescrived for pain control including muscular pain. Muscle atrophy is a disease that is characterized with a gradual muscle loss. Muscle atrophy is clearly observed in experimental animals that receive a repeated high-dose of an artificial glucocorticoid, dexamethasone (DEX). This transcriptome analysis aims to investigate the changes in global gene expression profiles in gastrocnemius (GA) and soleus (SO) muscle tissues from mice with DEX-induced muscle atrophy in the presence or absence of JGT co-treatment.

2023-03-21 | GSE227495 | GEO

Cetrorelix promotes cell apoptosis via the PI3K-AKT-FOXO1 pathway in epithelial ovarian cancer.

Project description: Not available

| S-EPMC12740856 | biostudies-literature

Gadd45a Promotes Skeletal Muscle Atrophy by Forming a Complex with the Protein Kinase MEKK4

Project description:Skeletal muscle atrophy is a serious and highly prevalent condition that remains poorly understood at the molecular level. Previous work found that skeletal muscle atrophy involves an increase in skeletal muscle Gadd45a expression, which is necessary and sufficient for skeletal muscle fiber atrophy. However, the direct mechanism by which Gadd45a promotes skeletal muscle atrophy was unknown. To address this question, we biochemically isolated skeletal muscle fiber proteins that associate with Gadd45a as it induces skeletal muscle atrophy in living mice. We found that Gadd45a interacts with multiple proteins in skeletal muscle fibers, including, most prominently, the MAP kinase kinase kinase MEKK4. Furthermore, by forming a complex with MEKK4 in skeletal muscle fibers, Gadd45a increases MEKK4 protein kinase activity, which is sufficient to induce skeletal muscle fiber atrophy and required for Gadd45a-mediated skeletal muscle fiber atrophy. Together, these results identify a direct biochemical mechanism by which Gadd45a induces skeletal muscle atrophy and provide new insight into way that skeletal muscle atrophy occurs at the molecular level.

2016-05-17 | MSV000079730 | MassIVE

3-iodothyronamine inhibits apoptosis induced by myocardial ischemia reperfusion via the Akt/FoxO1 signaling pathway.

Project description: Not available

| S-EPMC8908142 | biostudies-literature

N-Acetyl-L-Cysteine Reduces Cervical Carcinogenesis by Promoting Apoptosis.

Project description: Not available

| S-EPMC10293158 | biostudies-literature