Ask about this productRelated genes to: Fbxo32 Blocking Peptide
- Gene:
- FBXO32 NIH gene
- Name:
- F-box protein 32
- Previous symbol:
- -
- Synonyms:
- MAFbx, ATROGIN1, Fbx32
- Chromosome:
- 8q24.13
- Locus Type:
- gene with protein product
- Date approved:
- 2001-10-04
- Date modifiied:
- 2014-11-18
Related products to: Fbxo32 Blocking Peptide
Related articles to: Fbxo32 Blocking Peptide
- High-fat diets (HFDs) are a key contributor to obesity and promote oxidative stress and inflammation, which are associated with muscle atrophy and insulin resistance (IR). Passiflora edulis exhibits anti-obesity, antioxidant, and anti-inflammatory effects. The study aimed to investigate the potential benefit of P. edulis f. flavicarpa (PF) extract in preventing obesity-associated muscle atrophy and IR. The PF extract effectively inhibited cholesterol micelle solubility with an IC of 3431 µg/mL and decreased fat accumulation in 3T3-L1 adipocytes. Furthermore, this study investigated a model of HFD-induced IR and muscle atrophy in rats. Thirty-five male Sprague-Dawley (SD) rats were induced with obesity by HFD and were administered 250 and 500 mg/kg/day of PF extract. Rats fed with an HFD were associated with fat accumulation and oxidative stress, which promoted inflammation, muscle damage, muscle atrophy, and IR in obese rats. However, administration of PF extract effectively mitigated these effects. The PF extract decreased fat accumulation in white adipose tissues and gastrocnemius (GAS) muscle by inhibiting fat absorption and synthesis, particularly Cd36 and Hmgcr. The PF extract also notably reduced oxidative stress-induced muscle inflammation and damage via elevating nuclear factor erythroid 2-related factor 2 (Nrf2) and reducing nuclear factor kappa B (NF-κB) expressions. Additionally, PF extract was found to mechanistically prevent muscle atrophy by inhibiting Fbxo32, Trim63, and B-cell lymphoma 2 (BCL2)-associated X (Bax) expressions, while enhancing Bcl2 expression. We also found that PF extract mitigated muscle IR by upregulation of the insulin receptor substrate-1/phosphatidylinositol-3 kinase/protein kinase B (IRS-1/PI3K/AKT) pathway and Slc2a4 expression. The findings indicate that PF extract can prevent skeletal muscle loss and IR in obesity by modulating oxidative stress, inflammation, and activating IRS-1/PI3K/AKT signaling pathway. - Source: PubMed
Chobsuay NraratChonpathompikunlert PennapaSrivilai JukkarinMalakul WachirawadeeLimpeanchob NanteetipAimjongjun SathidTunsophon Sakara - Muscle atrophy, characterized by progressive loss of muscle mass and function, is driven by muscle-specific E3 ligases MAFbx and MuRF1. While transcriptional regulation of E3 ligases is documented, the mechanism of their regulation by the ubiquitin-proteasome system remains unclear. This study aims to identify a deubiquitinase (DUB) regulating these E3 ligases and reveal the mechanisms underlying the mitigation of muscle atrophy through inhibition of the discovered DUB. - Source: PubMed
Chae JongbeomWoo Seon MinSeo Seung UnYook SimmyungCho Hyo JeLee Jung YeolMin Kyoung JinPark JunhyeonRyu DongryeolKwon Taeg Kyu - Glucocorticoid-induced muscle atrophy involves accelerated protein breakdown and impaired regeneration. We evaluated the protective effects of heat-killed and live ANC4 against dexamethasone (Dex)-induced muscle wasting in C57BL/6 mice. Oral administration of ANC4 significantly improved grip strength and treadmill endurance while specifically preserving the mass of the gastrocnemius (GCM), a fast-twitch-dominant muscle. Mechanistically, ANC4 downregulated the glucocorticoid receptor (GR) and E3 ubiquitin ligases, including muscle RING-finger protein-1 (MuRF-1) and Atrogin-1, thereby mitigating catabolic signaling. Simultaneously, it up-regulated myogenic regenerative markers, including myogenic differentiation 1 (MyoD), myogenin, and myosin heavy chain (MyHC). Histological analysis confirmed that muscle fiber size restored and reduced fibrosis. Notably, the heat-killed form effectively increased MyHC, while the live form strongly suppressed Atrogin-1. These findings suggest that ANC4 prevents muscle atrophy by balancing catabolic signaling and myogenic repair, highlighting its potential as a probiotic or postbiotic therapy for preserving muscle mass and function. - Source: PubMed
Publication date: 2026/04/28
Hong Seong-MinPark JinhoKim Su-HyunHwang AhyoungJung Eun SungCho DonghyunJi YosepKim Sun YeouLee Choong-Hwan - Obesity is characterised by pathological alterations in visceral white adipose tissue (vWAT) that may contribute to the development of type 2 diabetes (T2D). While microRNAs (miRNAs) are key post-transcriptional regulators, comprehensive human vWAT profiling across metabolic states remains limited. This study characterised vWAT miRNA expression in lean, obese and obese+T2D individuals to identify obesity-driven regulatory networks associated with metabolic dysfunction. - Source: PubMed
Publication date: 2026/04/23
Villa-Fernández ElsaGarcía Ana VictoriaGallardo-Nuell LauraGarcía-Villarino MiguelFernández-García JuditMartin Alonso AldaraLozano-Aida ClaudiaSuárez Gutiérrez LorenaPujante PedroAres JessicaGonzález-Vidal TomásRodríguez Uría RaquelSanz Navarro SandraMoreno Gijón MaríaSanz Álvarez Lourdes MaríaTurienzo Santos Estrella OlgaFernández-Real José ManuelFernández Fraga MarioDelgado ElíasLambert Carmen - Sarcopenia lacks causal mechanisms and translatable targets. We integrated virtual gene knockout with multi-omics (n = 238 biopsies, 5 GEO cohorts) and single-cell RNA-seq (n = 10, 12,847 cells) to identify fibroblast-specific drivers. After ComBat batch correction, WGCNA identified a red module (690 genes, r = 0.74, P < 0.001) intersecting with 304 differentially expressed genes (|logFC|>0.585, FDR<0.05), yielding 163 candidates. scTenifoldKnk virtual gene knockout ranked PXDNL as the top fibroblast-specific driver (perturbation score = 2.34, CV<15%), perturbing 327 ECM genes (e.g., FBN1 ΔE = +0.82, LRRTM4 ΔE = -0.71). A 12-gene panel (including PXDNL) was derived from 113 ML algorithm benchmark (plsRglm optimal: training AUROC = 0.938, external validation AUROC = 0.804, 95%CI:0.636-0.938). Drug repurposing (DSigDB, Z > 2.0) identified GABA as the top candidate. Molecular docking revealed strong PXDNL-GABA binding (ΔG = -5.6 kcal/mol) at the peroxidase domain, which was further validated by enzymatic activity assays. In dexamethasone-induced and TNF-α induced atrophy models of CC or HMCs, 50 μM GABA restored cell viability (P < 0.001), downregulated Atrogin-1 (FBXO32)/MuRF-1 (TRIM63) (P < 0.01), and reversed PXDNL overexpression effects. This study establishes the fibroblast-PXDNL-ECM axis as a causal mechanism in sarcopenia and validates GABA as a repurposable therapeutic, providing a complete in silico-to-in vitro framework for age-related muscle disease. - Source: PubMed
Publication date: 2026/04/16
Cui Wei