Superoxide scavengers augment contractile but not energetic responses to hypoxia in rat diaphragm.

Acute exposure to severe hypoxia depresses contractile function and induces adaptations in skeletal muscle that are only partially understood. Previous studies have demonstrated that antioxidants (AOXs) given during hypoxia partially protect contractile function, but this has not been a universal finding. This study confirms that specific AOXs, known to act primarily as superoxide scavengers, protect contractile function in severe hypoxia. Furthermore, the hypothesis is tested that the mechanism of protection involves preservation of high-energy phosphates (ATP, creatine phosphate) and reductions of P(i). Rat diaphragm muscle strips were treated with AOXs and subjected to 30 min of hypoxia. Contractile function was examined by using twitch and tetanic stimulations and the degree of elevation in passive force occurring during hypoxia (contracture). High-energy phosphates were measured at the end of 30-min hypoxia exposure. Treatment with the superoxide scavengers 4,5-dihydroxy-1,3-benzenedisulfonic acid (Tiron, 10 mM) or Mn(III)tetrakis(1-methyl-4-pyridyl) porphyrin pentachloride (50 microM) suppressed contracture during hypoxia and protected maximum tetanic force. N-acetylcysteine (10 or 18 mM) had no influence on tetanic force production. Contracture during hypoxia without AOXs was also shown to be dependent on the extracellular Ca(2+) concentration. Although hypoxia resulted in only small reductions in ATP concentration, creatine phosphate concentration was decreased to approximately 10% of control. There were no consistent influences of the AOX treatments on high-energy phosphates during hypoxia. The results demonstrate that superoxide scavengers can protect contractile function and reduce contracture in hypoxia through a mechanism that does not involve preservation of high-energy phosphates.     

High energy phosphate concentrations and AMPK phosphorylation in skeletal muscle from mice with inherited differences in hypoxic exercise tolerance

The effect of chronic hypobaric hypoxia (1/2 atmospheric pressure) on high energy phosphate (HEP) compounds was investigated in slow (soleus; SOL) and fast twitch (extensor digitorum longus; EDL) muscle from 3 strains of mice with large differences in hypoxic exercise tolerance (HET). Phosphocreatine concentration ([PCr]) decreased 16–29% following hypoxia in EDL and SOL in all strains, while [ADP] and [AMP] increased. In the EDL, HET was negatively correlated with the PCr/ATP ratio and positively correlated with the ATP/P_i ratio. The free energy of ATP hydrolysis (ΔG_obs) remained constant despite the substantial changes that occurred in HEP profiles. The alteration of HEP set points and preservation of ΔG_obs are consistent with the notion that (1) maximal rates of steady-state ATP turnover are reduced under hypoxia, and (2) HEP perturbations during rest to work transitions are reduced in skeletal muscle from hypoxia acclimated animals. We therefore expected a lower phosphorylation ratio of AMP-activated protein kinase (AMPK-P/AMPK) during stimulation in hypoxic acclimated animals. However, neither the resting nor stimulated AMPK-P/AMPK was influenced by hypoxia, although there were significant differences among strains.     

藏羚羊骨骼肌肌红蛋白含量及乳酸脱氢酶、苹果酸脱氢酶活力的研究

目的:探讨藏羚羊骨骼肌对低氧环境的适应机制。方法:以生活在同海拔高度(4 300 m)的藏绵羊和低海拔绵羊(1 800 m)为对照,用分光光度法测定三种动物骨骼肌中肌红蛋白(Mb)含量、乳酸(LA)含量,酶活力法测定三种动物骨骼肌中乳酸脱氢酶(LDH)和苹果酸脱氢酶(MDH)活力。结果:藏羚羊骨骼肌中Mb含量明显高于藏绵羊和低海拔绵羊(P<0.05),而藏绵羊和低海拔绵羊间无明显差异。LA含量和LDH活力明显低于藏绵羊和低海拔绵羊(P<0.05),而MDH活力及MDH/LDH比值显著高于藏绵羊和低海拔绵羊(P<0.05),藏绵羊和低海拔绵羊间无明显差异。结论:藏羚羊可能通过增加骨骼肌中Mb的含量,提高其在低氧环境获取氧的能力,且藏羚羊骨骼肌组织中有氧代谢比例高,这可能与肌肉中Mb含量较高有关,推测藏羚羊较高的Mb含量可能是其适应高原缺氧条件的分子基础之一。     

Periods of systemic partial hypoxia induces apoptosis and inflammation in rat skeletal muscle

Critical illness myopathy (CIM) causes significant morbidity. In this study, we investigated the effect of repeated mild hypoxia on the skeletal muscle inflammation. Sprague–Dawley rats anesthetized with 2% inhaled isoflurane were divided into two groups (n = 6 each), normoxia and hypoxia (12.5% for 12 min followed by 35% for 12 min, at which point the cycle was repeated for three times). We measured the tissue oxygen tension and perfusion (simultaneously) in hind limb skeletal muscle. Inflammation in skeletal muscle was assessed by light microcopy (Hematoxylin-Eosin staining) and apoptosis (Fluorescein-FragEL DNA fragmentation detection) and expressed as percent normoxia. Compared to the control group, hypoxia significantly (P < 0.001) altered histomorphometrics. Similarly, DNA fragmentation analysis revealed that hypoxia significantly (P < 0.001) induced apoptosis. We conclude that after a mild but repeated hypoxic insult there is marked histological alterations and induced apoptosis in skeletal muscle. We postulate that variable periods of hypoxia in the critically ill may be playing a role in the etiology of CIM.     

低氧经mTOR/4E-BP1和FoxO1/Atrogin-1通路影响骨骼肌蛋白质积累

低氧暴露对骨骼肌蛋白质合成/分解的影响受到广泛关注,但该过程中相关调控通路的研究仍十分有限。本研究拟通过蛋白质相对积累量来研究合成和分解通路的变化。将骨骼肌细胞置于低氧环境中培养,分别在0 h、6 h、12 h和24 h收集细胞,并进行检测。免疫荧光观察肌球蛋白(myosin),翻译表面感应检测蛋白质合成,Western印迹法测试蛋白质合成相关基因(ERK1/2、p-ERK1/2、mTOR、p-mTOR、4E-BP1、p-4E-BP1)、蛋白质分解相关基因(泛素、FoxO1、p-FoxO1、MuRF1和Atrogin-1)表达量。结果发现,随着低氧干预时间延长,肌纤维直径和骨骼肌细胞中蛋白质相对积累量随时间逐渐减小(P<0.01)。与0 h相比,6 h p-4E-BP1/4E-BP1和Atrogin-1的表达显著上调(P<0.05),p-mTOR表达显著高于0 h(P<0.01);6 h和24 h p-mTOR/mTOR的比值显著大于0 h(P<0.05),而p-FoxO1/FoxO1的比值随时间逐渐减小(P<0.01)。上述结果表明,低氧干预能够使骨骼肌细胞直径减少、骨骼肌细胞蛋白质积累减少,并且低氧打破骨骼肌细胞蛋白质合成和分解的平衡,可能是通过调节mTOR/4E-BP1通路活性和FoxO1/Atrogin-1通路的活性实现的。     

The effect of thymus extracts on phosphorus compounds in muscle and serum, and on serum calcium

1. Thymectomy in young rabbits decreased the ATP content and increased the inorganic phosphate content of skeletal muscle. The serum calcium content was decreased, whereas the inorganic phosphate content was increased. 2. The administration of a lipid fraction (TL) or protein fractions (CIF and TP) of thymus extracts to thymectomized rabbits in short-term experiments increased the ATP content of muscle and decreased the inorganic phosphate contents of muscle and serum. Serum calcium content was increased. 3. The action of the thymus extract TP was specific only on the phosphate compounds, since the increase in serum calcium concentration was also caused by the control extract from muscle. The action of the extract TL is not specific, being paralleled by the action of a control extract from muscle.     

抗阻训练通过Akt-FoxO1通路抑制低氧诱导的骨骼肌萎缩

高原低氧环境会引起肌力下降和运动能力退化,而抗阻训练是刺激骨骼肌生长的重要手段,叉头转录因子1（fork head box protein O 1,FoxO1）在调控骨骼肌蛋白质分解通路中承担重要角色。为探究Akt-FoxO1通路是否参与抗阻训练抑制低氧诱导的骨骼肌萎缩,本研究构建低氧诱导骨骼肌萎缩的大鼠模型,并模拟海拔4 000 m低氧环境下（12.4% O2）进行抗阻训练,对比观察大鼠比目鱼肌和趾长伸肌湿重和横截面积,以及蛋白激酶B（protein kinase B,Akt）、叉头转录因子1、泛素蛋白连接酶1（muscle ring finger 1,MuRF1）的表达差异等。结果表明,低氧暴露导致大鼠趾长伸肌湿重显著下降,苏木精-伊红染色组织切片分析肌纤维横截面积、低氧环境下比目鱼肌横截面积明显下降,而低氧抗阻训练后趾长伸肌横截面积明显高于安静组。实时荧光定量PCR和蛋白质免疫印迹结果显示,低氧暴露后FoxO1和MuRF1基因表达明显上调,低氧下抗阻训练后发现,Akt基因表达明显上调而FoxO1、MuRF则明显下调。免疫荧光观察磷酸化FoxO1在细胞核内外表达情况,发现抗阻训练后FoxO1（S256）于细胞核外表达增强。上述结果表明,抗阻训练可以达到抑制低氧诱导骨骼肌萎缩的效果,Akt促进FoxO1磷酸化从而减缓骨骼肌蛋白质分解过程是抗阻训练能够抑制骨骼肌萎缩的分子机制之一。     

耐力训练抑制急性低氧时骨骼肌线粒体生物能学变化:ROS和UCP3的作用(英文)

骨骼肌线粒体解耦联蛋白3（uncoupling protein3,UCP3）在低氧时的生理作用尚不清楚。本研究观察了大鼠在耐力训练前后,模拟急性高原低氧各时间点的骨骼肌线粒体UCP3 mRNA和蛋白表达、线粒体呼吸功能、活性氧（reactive oxygen species,ROS）产生速率以及锰超氧化物歧化酶（manganese superoxide dismutase,MnSOD）表达和活性的变化。急性低氧导致线粒体一系列生物能学功能障碍。未训练大鼠UCP3蛋白在4h时比静息时升高了60％,而MnSOD蛋白含量及活性在低氧暴露过程中无显著变化;UCP3蛋白上调通过降低电子传递链耦联程度抑制O2-产生,但同时降低了ATP合成效率。耐力训练显著抑制急性低氧诱导的骨骼肌UCP3蛋白上调（67％;S42％）。训练组大鼠的ROS产生速率在低氧2h、4h和6h时显著低于未训练组;MnSOD蛋白含量及活性分别较术训练组提高了50％和34％。训练组人鼠MnSOD上调可增加线粒体对ROS的耐受力,进而抑制UCP3蛋白表达,从而提高氧化磷酸化效率。急性低氧中,未训练组大鼠呼吸控制比（respiratory control ratio,RCR）和磷氧比（ADP to oxygen consumption ratio,P／O）显著降低,而训练组RCR和P／O保持相对稳定。以上结果提示：（1）模拟急性高原低氧可诱导UCP3 mRNA及蛋白表达升高,从而降低升高了的线粒体膜电位（△ψ）,使ROS的产生减少;（2）耐力训练可抑制低氧诱导的UCP3表达上调,提高ROS酶学清除能力,从而提高线粒体氧化磷酸化效率。     

Phosphorus-31 nuclear magnetic resonance of phosphoenzymes of sodium- and potassium-activated and of calcium-activated adenosinetriphosphatase

Prior studies identified phosphoenzyme intermediates in the turnover of sodium- and potassium-activated adenosinetriphosphatase [(Na,K)ATPase] from several sources and of the calcium-activated adenosinetriphosphatase [(Ca)-ATPase] of skeletal muscle sarcoplasmic reticulum. In both cases, the transphosphorylation is to a beta-aspartyl carboxyl group at the active site. We now report observation of a K+-sensitive phosphorylated intermediate of purified (Na,-K)ATPase from the salt gland of the duck using high-field 31P nuclear magnetic resonance. Addition of ATP to a suspension of this enzyme in the presence of Mg2+ and Na+ produced a resonance at about +17 ppm relative to 85% phosphoric acid. Addition of inorganic phosphate and Mg2+ to (Na,K)ATPase also produced a resonance at about +17 ppm which was enhanced in the presence of a saturating concentration of the inhibitor, ouabain; again, addition of K+ made this resonance disappear. These findings are consistent with earlier kinetic characterization of an acid-stable (Na,K)ATPase phosphoenzyme intermediate by 32P-labeled phosphate incorporation into a denatured precipitate of the enzyme. We attribute the +17-ppm resonance to formation of an acyl phosphate at an aspartyl residue of the catalytic site of (Na,K)ATPase. This is supported by our finding of a similar resonance at +17 ppm after phosphorylation of another membrane-bound cation transport enzyme, sarcoplasmic reticulum (Ca)ATPase, as well as by a similar resonance at about +17 ppm after phosphorylation of the model dipeptide L-seryl-L-aspartate.     

A phosphorus-31 nuclear magnetic resonance study on the complex of chicken gizzard myosin subfragment 1 with adenosine diphosphate

The complex of Mg-ADP with chicken gizzard myosin subfragment 1 (S1), obtained by the treatment with Staphylococcus aureus V8 proteinase, was observed with 31P NMR at various temperatures between 0 and 25°C. The signal of S1·ADP complex was observed at -2 to -3 ppm as a rather broad peak. As compared with the results for rabbit skeletal muscle S1·ADP complex (Tanokura M, Ebashi S: J Biochem 113: 19-21, 1993), the signal was assigned to -phosphate of ADP in the S1·ADP complex. The signal of the complex was so broad and weak that the dependences on temperature and magnetic field strength were not clear. The observation suggests the tight interaction of S1 with the phosphate moieties of ADP in the complex and the extremely anisotropic distribution of electrons around phosphorus nuclei.     

小鼠不同组织及缺氧损伤后的大鼠心肌细胞中RIP3的表达

目的:检测小鼠组织中受体相互作用丝氨酸/苏氨酸蛋白激酶家族(RIPs)表达谱,并检测RIP3在大鼠心肌细胞缺氧损伤后的表达。方法:①采用荧光实时定量PCR分别检测RIPs家族基因在小鼠组织(心、肝、肺、肾、脑、小肠、骨骼肌、脾和主动脉)中的mRNA表达谱,并采用Western blot进一步检测RIP3在小鼠组织的蛋白表达谱。②将培养的大鼠心肌细胞分为缺氧组和对照组,缺氧组置于缺氧环境中培养48 h,采用western blot检测其中RIP3的表达变化。结果:①mRNA水平:RIP1 mRNA在脑组织中表达最高,心脏、肺、肾、骨骼肌较低;RIP2在心脏和肺表达量较其他组织高;RIP3在肠中表达较其他组织高出4倍以上,脑组织中未检测到RIP3表达;RIP4的表达以肺最高,而骨骼肌、脑和血管中表达量低。②蛋白水平:在小鼠组织中,RIP3表达以脑、骨骼肌中最高,心脏、肝、肺中表达较低。③培养的大鼠心肌细胞中,缺氧组心肌细胞的RIP3表达量显著高于对照组(P0.05)。结论:RIPs在小鼠组织中呈现差异表达,而在培养的大鼠心肌细胞缺氧损伤后RIP3表达升高。     

Temporal dynamics in growth and white skeletal muscle composition of the mummichog Fundulus heteroclitus during chronic hypoxia and hyperoxia

Specific growth rate (G(S) ) and white skeletal muscle composition were measured in the mummichog Fundulus heteroclitus over a period of 28 days at four levels of dissolved oxygen (DO): severe hypoxia (c. 1.2 mg O(2) l(-1) ), moderate hypoxia (3.0 mg O(2) l(-1) ), normoxia (7.1 mg O(2) l(-1) ) and hyperoxia (10.6 mg O(2) l(-1) ). The G(S) was calculated over 0-8, 0-14, 0-28 and 14-28 days, and muscle protein, lactate dehydrogenase (LDH), DNA, RNA and water were measured at 0, 8, 14 and 28 days. Exposure of fish to severe hypoxia was associated with significantly reduced G(S) , lower muscle protein content and lower RNA:DNA compared with other DO treatments. When calculated over the first and second half of the 28 day exposure, however, G(S) of fish in severe hypoxia increased significantly during the second two-week interval, to the same rate as that of normoxic fish. Muscle LDH activity and water content were not significantly affected by DO level. Neither moderate hypoxia nor hyperoxia significantly affected G(S) or any biochemical variable. The results demonstrate that F. heteroclitus can tolerate wide variation in ambient oxygen concentration and, during prolonged exposure to severe hypoxia, shows significant compensation for the initial negative effects on growth. The capacity of F. heteroclitus to grow over a wide range of DO probably contributes to its ability to exploit habitats characterized by marked variation in oxygen availability.     

Skeletal muscle capillarity and angiogenic mRNA levels after exercise training in normoxia and chronic hypoxia.

Gene expression of vascular endothelial growth factor (VEGF), and to a lesser extent of transforming growth factor-beta(1) (TGF-beta(1)) and basic fibroblast growth factor (bFGF), has been found to increase in rat skeletal muscle after a single exercise bout. In addition, acute hypoxia augments the VEGF mRNA response to exercise, which suggests that, if VEGF is important in muscle angiogenesis, hypoxic training might produce greater capillary growth than normoxic training. Therefore, we examined the effects of exercise training (treadmill running at the same absolute intensity) in normoxia and hypoxia (inspired O(2) fraction = 0.12) on rat skeletal muscle capillarity and on resting and postexercise gene expression of VEGF, its major receptors (flt-1 and flk-1), TGF-beta(1), and bFGF. Normoxic training did not alter basal or exercise-induced VEGF mRNA levels but produced a modest twofold increase in bFGF mRNA (P < 0.05). Rats trained in hypoxia exhibited an attenuated VEGF mRNA response to exercise (1.8-fold compared 3.4-fold with normoxic training; P < 0.05), absent TGF-beta(1) and flt-1 mRNA responses to exercise, and an approximately threefold (P < 0.05) decrease in bFGF mRNA levels. flk-1 mRNA levels were not significantly altered by either normoxic or hypoxic training. An increase in skeletal muscle capillarity was observed only in hypoxically trained rats. These data show that, whereas training in hypoxia potentiates the adaptive angiogenic response of skeletal muscle to a given absolute intensity of exercise, this was not evident in the gene expression of VEGF or its receptors when assessed at the end of training.     

Chronic hypoxia attenuates resting and exercise-induced VEGF, flt-1, and flk-1 mRNA levels in skeletal muscle.

Vascular endothelial growth factor (VEGF) is a hypoxia-inducible angiogenic mitogen. However, chronic hypoxia is generally not found to increase mammalian skeletal muscle capillarity. We sought to determine the effect of chronic hypoxia (8 wk, inspired O2 fraction = 0.12) on skeletal muscle gene expression of VEGF, its receptors (flt-1 and flk-1), basic fibroblast growth factor, and transforming growth factor-beta1. Wistar rats were exposed to chronic hypoxia (n = 12) or room air (n = 12). After the exposure period, six animals from each group were subjected to a single 1-h treadmill exercise bout (18 m/min on a 10 degrees incline) in room air while the remaining six animals served as rest controls. Morphological analysis revealed that chronic hypoxia did not increase skeletal muscle capillarity. Northern blot analyses showed that chronic hypoxia decreased resting VEGF, flt-1, and flk-1 mRNA by 23, 68, and 42%, respectively (P < 0.05). The VEGF mRNA response to exercise was also decreased (4.1- and 2.7-fold increase in room air and chronic hypoxia, respectively, P < 0.05). In contrast, neither transforming growth factor-beta1 nor basic fibroblast growth factor mRNA was significantly altered by chronic hypoxia. In conclusion, prolonged exposure to hypoxia attenuated gene expression of VEGF and its receptors flt-1 and flk-1 in rat gastrocnemius muscle. These findings may provide an explanation for the lack of mammalian skeletal muscle angiogenesis that is observed after chronic hypoxia.     

肌肉31P-MRS 的临床研究进展

磁共振波谱分析(magnetic resonance spectroscopy MRS)是目前唯一无创性定量研究人体组织细胞代谢、生理生化改变的方法。磁共振磷谱(31P-MRS)可对无机磷(Pi)、磷酸肌酸(PCr)、三磷酸腺苷(ATP)等含磷高能化合物进行定量分析,是在体研究骨骼肌能量代谢的有力工具。动态磷谱技术可测量肌肉在静息状态、收缩过程和恢复过程中细胞内高能磷酸化合物的变化,评价骨骼肌做功时的能量的转换效率,实现对线粒体功能的无创性评价。本文将对肌肉磷谱的研究进展做综述,尤其侧重于动态磷谱的应用,为以后利用磷谱客观研究肌肉相关疾病奠定良好的基础。     

The role of super-relaxed myosin in skeletal and cardiac muscle

The super-relaxed (SRX) state of myosin was only recently reported in striated muscle. It is characterised by a sub-population of myosin heads with a highly inhibited rate of ATP turnover. Myosin heads in the SRX state are bound to each other along the thick filament core producing a highly ordered arrangement. Upon activation, these heads project into the interfilament space where they can bind to the actin filaments. Thus far, the population and lifetimes of myosin heads in the SRX state have been characterised in rabbit cardiac, and fast and slow skeletal muscle, as well as in the skeletal muscle of the tarantula. These studies suggest that the role of SRX in cardiac and skeletal muscle regulation is tailored to their specific functions. In skeletal muscle, the SRX modulates the resting metabolic rate. Cardiac SRX represents a “reserve” of inactive myosin heads that may protect the heart during times of stress, e.g. hypoxia and ischaemia. These heads may also be called up when there is a sustained demand for increased power. The SRX in cardiac muscle provides a potential target for novel therapies.     

Effects of adenosine, exercise, and moderate acute hypoxia on energy substrate utilization of human skeletal muscle

Glucose metabolism increases in hypoxia and can be influenced by endogenous adenosine, but the role of adenosine for regulating glucose metabolism at rest or during exercise in hypoxia has not been elucidated in humans. We studied the effects of exogenous adenosine on human skeletal muscle glucose uptake and other blood energy substrates [free fatty acid (FFA) and lactate] by infusing adenosine into the femoral artery in nine healthy young men. The role of endogenous adenosine was studied by intra-arterial adenosine receptor inhibition (aminophylline) during dynamic one-leg knee extension exercise in normoxia and acute hypoxia corresponding to ～3,400 m of altitude. Extraction and release of energy substrates were studied by arterial-to-venous (A-V) blood samples, and total uptake or release was determined by the product of A-V differences and muscle nutritive perfusion measured by positron emission tomography. The results showed that glucose uptake increased from a baseline value of 0.2 ± 0.2 to 2.0 ± 2.2 μmol·100 g(-1)·min(-1) during adenosine infusion (P < 0.05) at rest. Although acute hypoxia enhanced arterial FFA levels, it did not affect muscle substrate utilization at rest. During exercise, glucose uptake was higher (195%) during acute hypoxia compared with normoxia (P = 0.058), and aminophylline had no effect on energy substrate utilization during exercise, despite that arterial FFA levels were increased. In conclusion, exogenous adenosine at rest and acute moderate hypoxia during low-intensity knee-extension exercise increases skeletal muscle glucose uptake, but the increase in hypoxia appears not to be mediated by adenosine.     

低氧运动对Nrf2基因敲除大鼠运动能力和氧化应激的影响

Nrf2可调节多种抗氧化酶的表达,Nrf2的缺失可能影响机体的运动能力,而低氧可提高机体的抗氧化能力并改善运动能力。为了考察低氧运动对Nrf2基因敲除大鼠运动能力和氧化应激的影响,本研究分别在常氧和低氧环境(12%氧浓度)中对野生型大鼠和Nrf2敲除大鼠进行4周的跑台运动。研究显示,低氧运动可提高野生型大鼠的跑台运动力竭时间,Nrf2敲除可缩短大鼠的力竭时间;低氧运动可上调大鼠的Nrf2 m RNA表达量;Nrf2敲除明显抑制HIF-1α蛋白表达,而低氧运动可上调野生型和Nrf2敲除大鼠的HIF-1α蛋白表达;Nrf2敲除大鼠的骨骼肌ROS水平明显升高,并且低氧均可降低野生型和Nrf2敲除大鼠骨骼肌ROS水平。低氧运动可上调Nrf2敲除大鼠的CAT和GSH-PX蛋白表达。苏木精和伊红(HE)染色显示,Nrf2敲除大鼠在力竭跑台运动完成后出现更严重的骨骼肌病理改变,而低氧运动可减轻骨骼肌损伤。本研究认为,Nrf2敲除导致了大鼠骨骼肌中抗氧化酶的抑制及ROS的过量累积,从而造成了骨骼肌损伤并降低了运动能力。此外,低氧可通过上调Nrf2的表达,进而激活HIF-1α及抗氧化酶活性,从而提高运动能力,并防止骨骼肌损伤。     

Tissue-specific stem cells: lessons from the skeletal muscle satellite cell

In 1961, the satellite cell was first identified when electron microscopic examination of skeletal muscle demonstrated a cell wedged between the plasma membrane of the muscle fiber and the basement membrane. In recent years it has been conclusively demonstrated that the satellite cell is the primary cellular source for muscle regeneration and is equipped with the potential to self renew, thus functioning as a bona fide skeletal muscle stem cell (MuSC). As we move past the 50(th) anniversary of the satellite cell, we take this opportunity to discuss the current state of the art and dissect the unknowns in the MuSC field.