UCP3

更新于：2025-01-23

基本信息

别名

Mitochondrial uncoupling protein 3、SLC25A9、Solute carrier family 25 member 9

+ [4]

简介

Putative transmembrane transporter that plays a role in mitochondrial metabolism via an as yet unclear mechanism (PubMed:21775425, PubMed:36114012). Originally, this mitochondrial protein was thought to act as a proton transmembrane transporter from the mitochondrial intermembrane space into the matrix, causing proton leaks through the inner mitochondrial membrane, thereby uncoupling mitochondrial membrane potential generation from ATP synthesis (PubMed:9305858, PubMed:11171965, PubMed:12670931, PubMed:12734183). However, this function is controversial and uncoupling may not be the function, or at least not the main function, but rather a consequence of more conventional metabolite transporter activity (PubMed:11707458).

关联

100 项与 UCP3 相关的临床结果

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100 项与 UCP3 相关的转化医学

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0 项与 UCP3 相关的专利（医药）

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1,546

项与 UCP3 相关的文献（医药）

2025-02-01·Journal of Cachexia, Sarcopenia and Muscle

Transcriptomic Profiling Reveals Differences in Slow‐Twitch and Fast‐Twitch Muscles of a Cigarette Smoke‐Exposed Rat Model

Article

作者: Wang, Xia ; Lau, Benson W. M. ; Ngai, Shirley P. C. ; Fung, Timothy K. H. ; Cheung, Kwok Kuen

ABSTRACTBackgroundCigarette smoking is known to affect muscle function and exercise capacity, including muscle fatigue resistance. Most studies showed diminished cross‐sectional area and fibre type shifting in slow‐twitch muscles such as the soleus, while effects on fast‐twitch muscles were seldom reported and the differential responses between muscle types in response to exposure to cigarette smoke (CS) were largely unknown. This study aimed to elucidate the histomorphological, biochemical and transcriptomic changes induced by CS on both slow‐twitch and fast‐twitch muscles.MethodMale Sprague–Dawley rats were randomly divided into two groups: sham air (SA) and CS. The rats were exposed to CS for 8 weeks using an exposure chamber system to mimic smoking conditions. Histomorphological analyses on muscle fibre type and cross‐sectional area were determined in soleus and extensor digitorum longus (EDL). Transcriptomic profiles were investigated for identifying differentially expressed genes (DEGs) and potential mechanistic pathways involved. Inflammatory responses in terms of the macrophage population and the level of inflammatory cytokines were measured. Markers for muscle‐specific proteolysis were also examined.ResultSoleus muscle, but not in EDL, exhibited a significant increase in Type IIa fibres (SA: 9.0 ± 3.3%; CS: 19.8 ± 2.4%, p = 0.002) and decrease in Type I fibres (SA: 90.1 ± 3.6%; CS: 77.9 ± 3.3%, p = 0.003) after CS exposure. RNA sequencing revealed 165 identified DEGs in soleus including upregulation of ‘Cd68’, ‘Ccl2’ and ‘Ucp2’ as well as downregulation of ‘Ucp3’, etc. Pathways enrichment analysis revealed that the upregulated pathways in soleus were related to immune system and cellular response, while the downregulated pathways were related to oxidative metabolism. Only 10 DEGs were identified in EDL with less enriched pathways. The soleus also showed elevated pro‐inflammatory cytokines, and the total macrophage marker CD68 was significantly higher in soleus of CS compared to the SA group (CD68+/no. of fibre: SA = 60.3 ± 39.3%; CS = 106.5 ± 27.2%, p = 0.0039), while the two groups in EDL muscle showed no significant difference. The expression of E3 ubiquitin ligase atrogin‐1 associated with muscle degradation pathways was 1.63‐fold higher in the soleus after CS, while no significant differences were observed in the EDL.ConclusionThe CS‐induced inflammatory responses on soleus muscle are likely mediated via targeting mitochondrial‐related signalling, resulting in mitochondrial dysfunction and impaired oxidative capacity. The presumably less active mitochondrial‐related signalling in EDL renders it less susceptible to changes towards CS, accounting for differential impacts between muscle types.

2025-02-01·Journal of Cachexia, Sarcopenia and Muscle

Lonafarnib Protects Against Muscle Atrophy Induced by Dexamethasone

Article

作者: Mun, Seyoung ; Bae, Sanghoon ; Han, Kyudong ; Mai, Van‐Hieu ; Hyun, Jung Keun ; Dong, Dalong ; Park, Sunghyouk

ABSTRACTBackgroundMuscle atrophy, including glucocorticoid‐induced muscle wasting from treatments such as dexamethasone (DEX), results in significant reductions in muscle mass, strength and function. This study investigates the potential of lonafarnib, a farnesyltransferase inhibitor, to counteract DEX‐induced muscle atrophy by targeting key signalling pathways.MethodsWe utilized in vitro models with C2C12 myotubes treated with DEX and in vivo models with Caenorhabditis elegans and DEX‐treated Sprague–Dawley rats. Myotube morphology was assessed by measuring area, fusion index and diameter. Muscle function was evaluated by grip strength and compound muscle action potential (CMAP) in the gastrocnemius (GC) and tibialis anterior (TA) muscles. Molecular mechanisms were explored through RNA sequencing and Western blotting to assess changes in mitochondrial function and muscle signalling pathways.ResultsLonafarnib (2 μM) significantly improved myotube area (1.49 ± 0.14 × 105 μm2 vs. 1.03 ± 0.49 × 105 μm2 in DEX, p < 0.05), fusion index (18.73 ± 1.23% vs. 13.3 ± 1.56% in DEX, p < 0.05) and myotube diameter (31.89 ± 0.89 μm vs. 21.56 ± 1.01 μm in DEX, p < 0.05) in C2C12 myotubes. In C. elegans, lonafarnib (100 μM) increased the pharyngeal pumping rate from 212 ± 7.21 contractions/min in controls to 308 ± 17.09 contractions/min at day 4 (p < 0.05), indicating enhanced neuromuscular function. In DEX‐induced atrophic rats, lonafarnib improved maximal grip strength (DEX: 13.91 ± 0.78 N vs. 1 μM lonafarnib: 16.18 ± 0.84 N and 5 μM lonafarnib: 16.71 ± 0.83 N, p < 0.05), increased muscle weight in GC, and enhanced CMAP amplitudes in both GC and TA muscles. Western blot analysis showed that lonafarnib treatment upregulated UCP3 and ANGPTL4 and increased phosphorylation of mTOR and S6 ribosomal protein (p < 0.05), indicating enhanced mitochondrial function and protein synthesis. Knockdown models further demonstrated that lonafarnib could partially rescue muscle atrophy phenotypes, indicating its action through multiple molecular pathways.ConclusionsLonafarnib mitigates dexamethasone‐induced muscle atrophy by enhancing mitochondrial function and activating anabolic pathways. These findings support further investigation of lonafarnib as a therapeutic agent for muscle atrophy in clinical settings.

2024-12-16·Animal Biotechnology

Dietary ginger ( Zingiber officinale ) enhances performance traits, biochemical and haematological indices of Turkey targeting mRNA gene expression

Article

作者: Ghanem, Hanaa M. ; Sakr, Abdelaziz M. ; Abdel-Latif, Mervat A. ; Ibraheim, Samya E. ; Manaa, Eman A. ; Albadrani, Ghadeer M. ; El Zawily, Amr ; Abdel-Daim, Mohamed M. ; Waheed, Rania M. ; Shafik, Basant M.

Ginger rich in polyphenols, possesses various biomedical properties. Researchers investigated the effects of dietary ginger supplementation on turkey performance traits, biochemical parameters, haematological parameters and mRNA gene expression. Ginger root powder was administered at different doses (0, 10, 20 and 40 g/kg) to the turkeys. Notably, the 20 g/kg group exhibited improved performance traits and a higher broiler production efficiency factor (BPEF). Importantly, ginger was found to be safe for turkeys based on serum indices. Furthermore, the expression of several growth-related genes, including growth hormone receptor (GHR), insulin-like growth factor 1 (IGF-1), adenine nucleotide translocase (ANT), cyclooxygenase 3 (COX-3) and uncoupling protein 3 (UCP-3), was upregulated in the 20 g/kg enhancing their growth performance and economic efficiency in addition to keeping their health status safe. Therefore, Ginger root powder can be supplemented for turkey at a concentration of 2% as the addition of ginger powder is a long-term process.

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