A systematic review of p53 regulation of oxidative stress in skeletal muscle.
A systematic review of p53 regulation of oxidative stress in skeletal muscle.
复制标题
DOI：
10.1080/13510002.2017.1416773
复制
发表时间：
2018-12
期刊：
影响因子：
--
通讯作者：
Hood DA
中科院分区：
文献类型：
--
作者：
Beyfuss K;Hood DA
背景：p53是一种肿瘤抑制蛋白，参与调节多种信号通路。p53在细胞中的作用取决于氧化应激的类型、强度和持续时间。过去十年的研究揭示了p53在介导氧化应激负荷中的双重功能。然而，这取决于所施加应力的具体性质，因此需要进一步分析。 方法：在电子检索Pubmed、Google Scholar和ScienceDirect数据库后进行系统综述。基于动物和细胞培养模型中骨骼肌中p53的分析，识别并分离了1990年1月1日至2017年3月1日期间以英语发表的文章。 结果如下：根据氧化应激的方式对文献进行分类，包括运动、饮食调整、外源性氧化剂、组织操作、辐照和缺氧。在低至中等水平的氧化应激下，p53参与激活增加细胞修复时间的途径，如细胞周期停滞和自噬，以提高细胞存活率。然而，随着应激强度和持续时间的增加，例如照射、缺氧和氧化剂，p53的作用会发生转变，通过启动DNA片段化来诱导细胞凋亡，从而促进细胞应激水平的增加，从而防止异常细胞增殖。 结论：目前的证据证实，p53作为一个阈值调节细胞内稳态。因此，在每种方式中，强度和持续时间是氧化应激的参数，必须进行分析，以确定p53在调节信号通路以维持骨骼肌细胞健康和功能中的作用。 缩略语：学院：酰基辅酶A脱氢酶，长链; Acadm：酰基辅酶A脱氢酶，C-4至C-12直链; AIF：凋亡诱导因子; Akt：蛋白激酶B（PK B）; AMPK：AMP活化蛋白激酶; ATF-4：转录激活因子4; ATM：ATM丝氨酸/苏氨酸激酶; Bax：BCL 2相关X，凋亡调节因子; Bcl-2：B细胞白血病/淋巴瘤2凋亡调节因子; Bhlhe40：碱性螺旋-环-螺旋家族成员e40; BH 3：硼烷; Bim：细胞死亡的bcl-2相互作用介质; Bok：Bcl-2相关卵巢杀伤细胞; COX-IV：细胞色素c氧化酶IV; cGMP：环鸟苷一磷酸; c-myc：原癌基因蛋白; Cpt1b：肉毒碱棕榈酰转移酶1B; Dr5：死亡受体5; eNOS：内皮型一氧化氮合酶; ERK：细胞外调节MAP激酶; Fas：Fas细胞表面死亡受体; FDXR：铁氧还蛋白还原酶; FOXO3a：叉头盒O3; Gadd45 a：生长停滞和DNA损伤诱导45 α; GLS 2：转氨酶2; GLUT 1和4：葡萄糖转运蛋白1（内皮）和4（骨骼肌）; GSH：谷氨酰胺; Hes 1：hes家族bHLH转录因子1; Hey 1：具有YRPW基序1的hes相关家族bHLH转录因子; HIFI-α：缺氧诱导因子1，α-亚基; HK 2：己糖激酶2; HSP 70：热休克蛋白70;过氧化氢：双氧水; Id 2：DNA结合2抑制剂; IGF-1-BP3：胰岛素样生长因子结合蛋白3; IL-1 β：白细胞介素1 β; iNOS：诱导型一氧化氮合酶; IRS-1：胰岛素受体底物1; JNK：c-Jun N-末端激酶; LY-83583：6-苯胺基-5，8-喹啉二酮;可溶性鸟苷酸环化酶和cGMP生成抑制剂; Mdm 2/4：Mdm 4（人类）; mtDNA：线粒体DNA; MURF 1：肌肉环指蛋白-1; MyoD：肌细胞分化1; MyoG：肌细胞生成素; Nanog：Nanog同源框; NF-κ B：核因子-κ B; NO：一氧化氮; NoxA：佛波醇-12-肉豆蔻酸-13-乙酸诱导蛋白1（Pmaip 1）; NRF-1：核呼吸因子1; Nrf2：核因子红细胞2相关因子2; P21：Cdkn1a细胞周期蛋白依赖性激酶抑制剂1A（P21）; P38 MAPK：丝裂原活化蛋白激酶; p53 R2：p53诱导型核糖核苷酸还原酶基因; P66 Shc：含src同源2结构域的转化蛋白C1; PERP：与PMP-22相关的p53凋亡效应因子; PGC-1 α：过氧化物酶体增殖物激活受体γ共激活因子1-α; PGM：磷酸葡萄糖变位酶; PI3K：磷脂酰肌醇-4，5-二磷酸3-激酶; PKC β：蛋白激酶c β; PTEN：磷酸酶和张力蛋白同源物; PTIO：2-苯基-4，4，5，5-四甲基咪唑啉-1-氧基3-氧化物（PTIO）已用作一氧化氮（NO）清除剂; Puma：p53上调的凋亡调节剂; PW1：父本表达3（Peg3）; RNS：活性氮物质; SIRT 1：沉默调节蛋白1; SCO2：细胞色素c氧化酶组装蛋白; SOD 2：超氧化物歧化酶2; Tfam：线粒体转录因子A; TIGAR：Trp53诱导的糖酵解阻遏磷酸酶; TNF-α：肿瘤坏死因子α; TRAF 2：TNF受体相关因子2; TRAIL：II型跨膜蛋白。
Background: p53 is a tumor suppressor protein involved in regulating a wide array of signaling pathways. The role of p53 in the cell is determined by the type of imposed oxidative stress, its intensity and duration. The last decade of research has unravelled a dual nature in the function of p53 in mediating the oxidative stress burden. However, this is dependent on the specific properties of the applied stress and thus requires further analysis. Methods: A systematic review was performed following an electronic search of Pubmed, Google Scholar, and ScienceDirect databases. Articles published in the English language between January 1, 1990 and March 1, 2017 were identified and isolated based on the analysis of p53 in skeletal muscle in both animal and cell culture models. Results: Literature was categorized according to the modality of imposed oxidative stress including exercise, diet modification, exogenous oxidizing agents, tissue manipulation, irradiation, and hypoxia. With low to moderate levels of oxidative stress, p53 is involved in activating pathways that increase time for cell repair, such as cell cycle arrest and autophagy, to enhance cell survival. However, with greater levels of stress intensity and duration, such as with irradiation, hypoxia, and oxidizing agents, the role of p53 switches to facilitate increased cellular stress levels by initiating DNA fragmentation to induce apoptosis, thereby preventing aberrant cell proliferation. Conclusion: Current evidence confirms that p53 acts as a threshold regulator of cellular homeostasis. Therefore, within each modality, the intensity and duration are parameters of the oxidative stressor that must be analyzed to determine the role p53 plays in regulating signaling pathways to maintain cellular health and function in skeletal muscle. Abbreviations: Acadl: acyl-CoA dehydrogenase, long chain; Acadm: acyl-CoA dehydrogenase, C-4 to C-12 straight chain; AIF: apoptosis-inducing factor; Akt: protein kinase B (PKB); AMPK: AMP-activated protein kinase; ATF-4: activating transcription factor 4; ATM: ATM serine/threonine kinase; Bax: BCL2 associated X, apoptosis regulator; Bcl-2: B cell Leukemia/Lymphoma 2 apoptosis regulator; Bhlhe40: basic helix-loop-helix family member e40; BH3: Borane; Bim: bcl-2 interacting mediator of cell death; Bok: Bcl-2 related ovarian killer; COX-IV: cytochrome c oxidase IV; cGMP: Cyclic guanosine monophosphate; c-myc: proto-oncogene protein; Cpt1b: carnitine palmitoyltransferase 1B; Dr5: death receptor 5; eNOS: endothelial nitric oxide synthase; ERK: extracellular regulated MAP kinase; Fas: Fas Cell surface death receptor; FDXR: Ferredoxin Reductase; FOXO3a: forkhead box O3; Gadd45a: growth arrest and DNA damage-inducible 45 alpha; GLS2: glutaminase 2; GLUT 1 and 4: glucose transporter 1(endothelial) and 4 (skeletal muscle); GSH: Glutathione; Hes1: hes family bHLH transcription factor 1; Hey1: hes related family bHLH transcription factor with YRPW motif 1; HIFI-α: hypoxia-inducible factor 1, α-subunit; HK2: Hexokinase 2; HSP70: Heat Shock Protein 70; H2O2: Hydrogen Peroxide; Id2: inhibitor of DNA-binding 2; IGF-1-BP3: Insulin-like growth factor binding protein 3; IL-1β: Interleukin 1 beta; iNOS: inducible nitric oxide synthase; IRS-1: Insulin receptor substrate 1; JNK: c-Jun N-terminal kinases; LY-83583: 6-anilino-5,8-quinolinedione; inhibitor of soluble guanylate cyclase and of cGMP production; Mdm 2/ 4: Mouse double minute 2 homolog (mouse) Mdm4 (humans); mtDNA: mitochondrial DNA; MURF1: Muscle RING-finger protein-1; MyoD: Myogenic differentiation 1; MyoG: myogenin; Nanog: Nanog homeobox; NF-kB: Nuclear factor-κB; NO: nitric oxide; NoxA: phorbol-12-myristate-13-acetate-induced protein 1 (Pmaip1); NRF-1: nuclear respiratory factor 1; Nrf2: Nuclear factor erythroid 2-related factor 2; P21: Cdkn1a cyclin-dependent kinase inhibitor 1A (P21); P38 MAPK: mitogen-activated protein kinases; p53R2: p53 inducible ribonucleotide reductase gene; P66Shc: src homology 2 domain-containing transforming protein C1; PERP: p53 apoptosis effector related to PMP-22; PGC-1α: Peroxisome proliferator-activated receptor gamma coactivator 1-alpha; PGM: phosphoglucomutase; PI3K: Phosphatidylinositol-4,5-bisphosphate 3-kinase; PKCβ: protein kinase c beta; PTEN: phosphatase and tensin homolog; PTIO: 2-phenyl-4, 4, 5, 5,-tetramethylimidazoline-1-oxyl 3-oxide (PTIO) has been used as a nitric oxide (NO) scavenger; Puma: The p53 upregulated modulator of apoptosis; PW1: paternally expressed 3 (Peg3); RNS: Reactive nitrogen species; SIRT1: sirtuin 1; SCO2: cytochrome c oxidase assembly protein; SOD2: superoxide dismutase 2; Tfam: transcription factor A mitochondrial; TIGAR: Trp53 induced glycolysis repulatory phosphatase; TNF-a: tumor necrosis factor a; TRAF2: TNF receptor associated factor 2; TRAIL: type II transmembrane protein.
登录
查看更多内容
DOI：
10.1152/physiol.00010.2011
发表时间：
2011-08
期刊：
Physiology (Bethesda, Md.)
影响因子：
--
作者：
Cantó C;Auwerx J
通讯作者：
Auwerx J
p53的S-亚硝基化改变是导致衰老过程中骨骼肌中抗氧化剂反应受损的。
DOI：
10.18632/aging.101139
发表时间：
2016-12-20
期刊：
Aging
影响因子：
--
作者：
Baldelli S;Ciriolo MR
通讯作者：
Ciriolo MR
影响因子：
11.4
作者：
Bensaad, Karim;Cheung, Eric C.;Vousden, Karen H.
通讯作者：
Vousden, Karen H.
影响因子：
4.8
作者：
Di Carlo, A;De Mori, R;Germani, A
通讯作者：
Germani, A
影响因子：
3.3
作者：
Bartlett, Jonathan D.;Joo, Chang Hwa;Morton, James P.
通讯作者：
Morton, James P.