Ontology highlight
ABSTRACT:
PROVIDER: PRJNA899596 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22240304_1.fastq.gz | Fastqsanger.gz | |||
| SRR22240304_2.fastq.gz | Fastqsanger.gz | |||
| SRR22240305_1.fastq.gz | Fastqsanger.gz | |||
| SRR22240305_2.fastq.gz | Fastqsanger.gz | |||
| SRR22240306_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 6 |
Similar Datasets
Project description:Background and objectives: Current clinical interventions lack effective strategies to arrest temporomandibular joint osteoarthritis (TMJOA) progression. Emerging evidence highlights the therapeutic potential of microRNAs (miRNAs) in osteoarthritis (OA) management, though critical challenges persist regarding delivery efficiency, including unsatisfactory cellular uptake, immunogenicity, and structural instability of miRNA-based therapeutics. Methods and results: Considering the powerful editability of tetrahedral framework nucleic acids (tFNAs) for gene delivery, we engineered a novel nanoscale gene delivery system using tetrahedral framework nucleic acids functionalized with miR-143-3p (tFNAs-143). Through comprehensive in vivo modeling of TMJOA destabilization and in vitro simulation of IL-1β-induced inflammatory microenvironments, we systematically investigated the therapeutic efficacy and molecular mechanisms underlying OA pathophysiology of tFNAs-143. Our results demonstrated that tFNAs-143 exhibited excellent cellular internalization in chondrocytes and effectively mitigated TMJOA progression by impeding ferritinophagy-mediated ferroptosis. Conclusions: This study advanced miRNA delivery technology for TMJOA therapy, deepened the insights into TMJOA pathogenesis, and proposed a promising nano therapeutic strategy for developing targeted TMJOA therapies.
2026-01-21 | GSE303194 | GEO
Project description:Tetrahedral framework nucleic acids loaded siCCR2 restrains M1 macrophage polarization to ameliorate pulmonary fibrosis in chemoradiation-induced murine model
| PRJNA1065377 | ENA
Project description:The sarcopenia-associated decline of the muscular performances in older people is improved<br>by exercise and caloric restriction but is still lacking a more suitable pharmacological<br>treatment. We investigated the effects of EGb 761, a Gingko biloba extract used to treat<br>chronic age-dependent neurological disorders, on the soleus muscle of aged rats. DNA<br>microarray analysis shows that the EGb 761 treatment is associated with the transcriptional<br>reprogramming of genes related to regeneration and energy production functions. EGb 761<br>up-regulated genes implicated in myogenesis though the TGF? signaling pathway. Also, EGb<br>761, by modulating genes implicated in fatty acids and glucose oxidation, reversed the agerelated<br>shift from lipids to glucose and improved energy production in mitochondria. These<br>modifications restore a more juvenile gene expression pattern that is concomitant with the<br>improvement of the muscular performances, as assessed by electrophysiological and<br>biochemical parameters. Thus, EGb 761 may represent a novel treatment for sarcopenia
2009-06-30 | E-MEXP-1937 | biostudies-arrayexpress
Project description:The degenerative loss of muscle associated with aging leading to muscular atrophy is called sarcopenia. Currently, practicing regular physical exercise is the only efficient way to delay the onset of sarcopenia. To identify therapeutic targets to suppress the symptoms of aging, there is a need for in vivo model organisms of accelerated muscle degeneration and atrophy. The zebrafish harbors hallmarks of aging, notably mitochondrial dysfunction, telomeres shortening and accumulation of senescent cells. Unfortunately, zebrafish aged slowly, and no specific zebrafish models of accelerated muscle atrophy associated with aging or sarcopenia are currently available. We have developed a new genetic tool to efficiently accelerate muscle fibers degeneration and muscle tissue atrophy in zebrafish larvae and adults. We used a gain-of-function strategy with a molecule that has been shown to be necessary and sufficient to induce muscle atrophy and a sarcopenia phenotype in mammals: Atrogin1 (also named Fbxo32). We report the generation, validation, and characterization of a zebrafish genetic model of accelerated muscle atrophy, the sarcofish. We demonstrated that specific expression of Atrogin1 in skeletal muscle tissue induces a muscle atrophic phenotype associated with locomotion dysfunctions in both larvae and adult fish. We identified that degradation of the myosin light chain as an event occurring before the degeneration of muscle fibers. Biological processes associated with muscle aging such as inflammation, proteolysis, apoptosis and stress response are upregulated in the sarcofish. Surprisingly, we observed a strong correlation between muscle fibers degeneration and a reduction of neuromuscular junctions in the peripheral nervous system, as well as neuronal cell bodies in the spinal cord, suggesting that muscle atrophy could underly a neurodegenerative phenotype in the central nervous system. Finally, while sarcofish larvae harbor regeneration of muscle fibers, spinal neurons and recover locomotive functions, adult sarcofish have impaired regenerative capacities as observed in mammals during muscle aging. In the future, the sarcofish could open new strategies in the fight against the sarcopenia disease to test therapeutic molecules aiming to treat or alleviate the symptoms of muscle aging.
2024-08-09 | GSE274353 | GEO
Project description:Skeletal muscle-specific ablation of thyroid hormone receptor alpha (TRalpha) in young mice is sufficient to recapitulate key phenotypic hallmarks of age-related sarcopenia—including myofiber atrophy, exercise intolerance, and mitochondrial quality control failure—establishing receptor decline as a cell-autonomous driver of sarcopenia pathogenesis rather than a passive biomarker. The underlying mechanism reveals how systemic endocrine signals culminate in organelle-specific quality control defects: TRalpha transcriptionally drives the RNA-binding protein CLUH, which facilitates the perimitochondrial enrichment of Pink1 mRNA for localized synthesis of the mitophagy-initiating kinase. Consequently, TRalpha loss disrupts perimitochondrial Pink1 mRNA localization, impairing local PINK1 abundance and mitophagic priming, leading to accumulation of damaged mitochondria. Restoring CLUH expression rescues Pink1 mRNA spatial localization, mitophagy flux, and cellular senescence markers in both TRalpha-deficient myofibers and naturally aged muscle cells. These findings identify spatial transcriptome organization as an underappreciated regulatory layer in muscle wasting and provide a genetically defined framework linking endocrine decline to organelle-level post-transcriptional regulation.
2026-02-05 | GSE318551 | GEO
Project description:To elaborate the process of denervated muscular atrophy, and provide scientific basis for the prevention and treatment of denervated muscular atrophy. we performed a time course transcriptomic analysis of denervated muscular atrophy
2019-06-16 | E-MTAB-8009 | biostudies-arrayexpress
Project description:Nano MiRNA-Functionating Tetrahedral Framework Nucleic Acid for Cartilage-targeted Ferritinophagy Modulation to Attenuate Temporomandibular Joint Osteoarthritis
| PRJNA1294315 | ENA
Project description:The innervation of skeletal myofibers exerts a crucial influence on the maintenance of muscle tone and normal operation, but little is known concerning atrophy and its underlying mechanisms in denervated muscle to date. Here, we reported that activated NOD-like receptor protein 3 (NLRP3) inflammasome with pyroptotic cell death occurred in denervated gastrocnemius in the mouse model of sciatic denervation. This damage causes interleukin 1 beta (IL-1β) release，facilitating the ubiquitin proteasome system (UPS) activation, which was responsible for muscle proteolysis. Conversely, genetic knock-out of muscular NLRP3 inhibited the pyroptosis-associated protein expression and ameliorate muscle atrophy significantly. Meanwhile, co-treatment with shRNA-NLRP3, also remarkably attenuated NLRP3 inflammasome activator (NIA)-induced C2C12 myotube pyroptosis and atrophy. Interestingly, we also observed a correlation between NLRP3 inflammasome activation and muscular apoptosis possibly via caspase 1 mediation after denervation. This work for the first time elucidates on the roles and mechanisms of NLRP3 inflammasome in skeletal muscle atrophy during denervation and suggests the potential contribution to the pathogenesis of neuromuscular diseases.
2022-12-29 | GSE201133 | GEO
Project description:Pancreatic Ductal AdenoCarcinoma (PDAC), the most common pancreatic cancer, is a deadly cancer since it is often diagnosed late and resistant to current therapies. A large proportion of PDAC patients are affected by tumor-induced cachexia. This cachexia, characterized by a loss of muscle mass and strength (sarcopenia), contributes to patient frailty and poor therapeutic response. We have shown that mitochondrial metabolism is reprogrammed in PDAC tumors and constitutes a vulnerability, opening new therapeutic avenues. The objective of this work was to study the molecular mechanisms underlying mitochondrial remodeling in PDAC cachectic skeletal muscle. Our study focused on the gastrocnemius muscle of genetically-engineered mice spontaneously developing an autochthonous pancreatic tumor and cachexia (KIC GEMM). We compared KIC mice developing a pancreatic tumor in 9-11 weeks to control littermates. We performed an integrative study combining in vivo functional analyses by non-invasive Magnetic Resonance, and ex-vivo histology, Seahorse, RNA-sequencing, and proteomic mass spectrometry and Western blotting analyses. KIC cachectic PDAC mice exhibit severe sarcopenia with loss of muscle mass and strength associated with reduced muscle fiber’s size and induction of protein degradation processes. Mitochondrial alterations in skeletal muscle play a central role in PDAC-induced cachexia. Muscle atrophy is associated with strong mitochondrial metabolic defects that are not limited to carbohydrates and protein metabolism, but concern also lipids, ROS and nucleic acids. Our data provide a framework to guide towards the most relevant molecular markers that would be affected early in tumor development and could be targeted in the clinic to limit PDAC-induced cachexia at early stages of the pathology.
2024-03-11 | GSE226898 | GEO