Activation of senescence and aging characteristics by mitochondrially generated ROS: how are they linked?
作者信息
Papaconstantinou John, Hsieh Ching-Chyuan
出版信息
Cell Cycle. 2010 Oct 1;9(19):3831-3. doi: 10.4161/cc.9.19.13324. Epub 2010 Oct 11.
Abstract
摘要
相似文献
1
Activation of senescence and aging characteristics by mitochondrially generated ROS: how are they linked?线粒体产生的活性氧对衰老和老化特征的激活作用：它们是如何联系的？
Cell Cycle. 2010 Oct 1;9(19):3831-3. doi: 10.4161/cc.9.19.13324. Epub 2010 Oct 11.
2
Dermal fibroblasts from long-lived Ames dwarf mice maintain their in vivo resistance to mitochondrial generated reactive oxygen species (ROS).来自长寿艾姆斯侏儒小鼠的真皮成纤维细胞维持其对线粒体产生的活性氧（ROS）的体内抗性。
Aging (Albany NY). 2009 Jul 31;1(9):784-802. doi: 10.18632/aging.100077.
3
The ASK1-Signalosome regulates p38 MAPK activity in response to levels of endogenous oxidative stress in the Klotho mouse models of aging.在衰老的Klotho小鼠模型中，ASK1信号体响应内源性氧化应激水平调节p38丝裂原活化蛋白激酶活性。
Aging (Albany NY). 2010 Sep;2(9):597-611. doi: 10.18632/aging.100194.
4
Linking Klotho, Nrf2, MAP kinases and aging.连接klotho、Nrf2、丝裂原活化蛋白激酶与衰老
Aging (Albany NY). 2010 Oct;2(10):632-3. doi: 10.18632/aging.100219.
5
Thioredoxin-ASK1 complex levels regulate ROS-mediated p38 MAPK pathway activity in livers of aged and long-lived Snell dwarf mice.硫氧还蛋白-ASK1复合物水平调节衰老和长寿的斯内尔侏儒小鼠肝脏中ROS介导的p38丝裂原活化蛋白激酶途径活性。
FASEB J. 2006 Feb;20(2):259-68. doi: 10.1096/fj.05-4376com.
6
Redox control of cell death.细胞死亡的氧化还原调控
Antioxid Redox Signal. 2002 Jun;4(3):405-14. doi: 10.1089/15230860260196209.
7
Tumor necrosis factor-alpha and apoptosis signal-regulating kinase 1 control reactive oxygen species release, mitochondrial autophagy, and c-Jun N-terminal kinase/p38 phosphorylation during necrotizing enterocolitis.肿瘤坏死因子-α和凋亡信号调节激酶 1 控制活性氧释放、线粒体自噬以及坏死性小肠结肠炎中 c-Jun N-末端激酶/p38 磷酸化。
Oxid Med Cell Longev. 2009 Nov-Dec;2(5):297-306. doi: 10.4161/oxim.2.5.9541.
8
Apoptosis signal regulating kinase-1 connects reactive oxygen species to p38 MAPK-induced mitochondrial apoptosis in UVB-irradiated human keratinocytes.凋亡信号调节激酶-1在紫外线B照射的人角质形成细胞中将活性氧与p38丝裂原活化蛋白激酶诱导的线粒体凋亡联系起来。
Free Radic Biol Med. 2006 Nov 1;41(9):1361-71. doi: 10.1016/j.freeradbiomed.2006.07.007. Epub 2006 Jul 15.
9
Redox Regulation of Cardiac ASK1 (Apoptosis Signal-Regulating Kinase 1) Controls p38-MAPK (Mitogen-Activated Protein Kinase) and Orchestrates Cardiac Remodeling to Hypertension.氧化还原调控心脏 ASK1（凋亡信号调节激酶 1）控制 p38-MAPK（丝裂原活化蛋白激酶）并协调高血压心脏重构。
Hypertension. 2020 Oct;76(4):1208-1218. doi: 10.1161/HYPERTENSIONAHA.119.14556. Epub 2020 Sep 9.
10
Redox cycling of 1,2-naphthoquinone by thioredoxin1 through Cys32 and Cys35 causes inhibition of its catalytic activity and activation of ASK1/p38 signaling.通过半胱氨酸 32 和 35 位的硫氧还蛋白 1 实现 1,2-萘醌的氧化还原循环，会抑制其催化活性并激活 ASK1/p38 信号通路。
Chem Res Toxicol. 2012 Jun 18;25(6):1222-30. doi: 10.1021/tx300069r. Epub 2012 Jun 1.
引用本文的文献
1
Anthocyanin-Binding Affinity and Non-Covalent Interactions with IIS-Pathway-Related Protein Through Molecular Docking.通过分子对接研究花青素结合亲和力及其与胰岛素/胰岛素样生长因子信号通路（IIS通路）相关蛋白的非共价相互作用
Curr Issues Mol Biol. 2025 Jan 29;47(2):87. doi: 10.3390/cimb47020087.
2
Aging, oxidative stress and degenerative diseases: mechanisms, complications and emerging therapeutic strategies.衰老、氧化应激与退行性疾病：机制、并发症与新兴治疗策略。
Biogerontology. 2023 Oct;24(5):609-662. doi: 10.1007/s10522-023-10050-1. Epub 2023 Jul 30.
3
Oxidative Stress and Energy Metabolism in the Brain: Midlife as a Turning Point.大脑中的氧化应激与能量代谢：中年作为一个转折点
Antioxidants (Basel). 2021 Oct 28;10(11):1715. doi: 10.3390/antiox10111715.
4
Involvement of p38 MAPK in Synaptic Function and Dysfunction.p38MAPK 在突触功能和功能障碍中的作用。
Int J Mol Sci. 2020 Aug 6;21(16):5624. doi: 10.3390/ijms21165624.
5
The Role of Signaling Pathways of Inflammation and Oxidative Stress in Development of Senescence and Aging Phenotypes in Cardiovascular Disease.炎症和氧化应激信号通路在心血管疾病衰老表型发生发展中的作用。
Cells. 2019 Nov 4;8(11):1383. doi: 10.3390/cells8111383.
6
Knockdown of PRL-3 increases mitochondrial superoxide anion production through transcriptional regulation of RAP1.抑制PRL-3通过对RAP1的转录调控增加线粒体超氧阴离子的产生。
Cancer Manag Res. 2018 Oct 30;10:5071-5081. doi: 10.2147/CMAR.S165344. eCollection 2018.
7
p38 Mitogen activated protein kinase (MAPK): a new therapeutic target for reducing the risk of adverse pregnancy outcomes.p38丝裂原活化蛋白激酶（MAPK）：降低不良妊娠结局风险的新治疗靶点。
Expert Opin Ther Targets. 2016 Dec;20(12):1397-1412. doi: 10.1080/14728222.2016.1216980. Epub 2016 Aug 4.
8
Attenuation of p38α MAPK stress response signaling delays the in vivo aging of skeletal muscle myofibers and progenitor cells.p38α丝裂原活化蛋白激酶应激反应信号的减弱会延缓骨骼肌肌纤维和祖细胞的体内衰老。
Aging (Albany NY). 2015 Sep;7(9):718-33. doi: 10.18632/aging.100802.
9
Senescence of primary amniotic cells via oxidative DNA damage.通过氧化 DNA 损伤使原代羊膜细胞衰老。
PLoS One. 2013 Dec 27;8(12):e83416. doi: 10.1371/journal.pone.0083416. eCollection 2013.
10
STAT5 triggers BCR-ABL1 mutation by mediating ROS production in chronic myeloid leukaemia.信号转导及转录激活因子5（STAT5）通过介导慢性髓性白血病中的活性氧生成触发BCR-ABL1突变。
Oncotarget. 2012 Dec;3(12):1669-87. doi: 10.18632/oncotarget.806.
本文引用的文献
1
Mechanism of oxidative stress-induced ASK1-catalyzed MKK6 phosphorylation.氧化应激诱导 ASK1 催化 MKK6 磷酸化的机制。
Biochemistry. 2010 May 18;49(19):4094-102. doi: 10.1021/bi100010j.
2
Dermal fibroblasts from long-lived Ames dwarf mice maintain their in vivo resistance to mitochondrial generated reactive oxygen species (ROS).来自长寿艾姆斯侏儒小鼠的真皮成纤维细胞维持其对线粒体产生的活性氧（ROS）的体内抗性。
Aging (Albany NY). 2009 Jul 31;1(9):784-802. doi: 10.18632/aging.100077.
3
p38MAPK controls expression of multiple cell cycle inhibitors and islet proliferation with advancing age.随着年龄增长，p38丝裂原活化蛋白激酶（p38MAPK）控制多种细胞周期抑制剂的表达及胰岛增殖。
Dev Cell. 2009 Jul;17(1):142-9. doi: 10.1016/j.devcel.2009.05.009.
4
Serine 58 of 14-3-3zeta is a molecular switch regulating ASK1 and oxidant stress-induced cell death.14-3-3ζ蛋白的丝氨酸58是调节ASK1和氧化应激诱导的细胞死亡的分子开关。
Mol Cell Biol. 2009 Aug;29(15):4167-76. doi: 10.1128/MCB.01067-08. Epub 2009 May 18.
5
Chemical biology investigation of cell death pathways activated by endoplasmic reticulum stress reveals cytoprotective modulators of ASK1.对内质网应激激活的细胞死亡途径的化学生物学研究揭示了ASK1的细胞保护调节剂。
J Biol Chem. 2009 Jan 16;284(3):1593-603. doi: 10.1074/jbc.M807308200. Epub 2008 Nov 12.
6
Role of TGF-beta1-independent changes in protein neosynthesis, p38alphaMAPK, and cdc42 in hydrogen peroxide-induced senescence-like morphogenesis.转化生长因子-β1非依赖性的蛋白质新合成、p38α丝裂原活化蛋白激酶和细胞分裂周期蛋白42变化在过氧化氢诱导的衰老样形态发生中的作用
Free Radic Biol Med. 2008 May 1;44(9):1732-51. doi: 10.1016/j.freeradbiomed.2008.01.026. Epub 2008 Feb 12.
7
Redox control of cell fate by MAP kinase: physiological roles of ASK1-MAP kinase pathway in stress signaling.丝裂原活化蛋白激酶对细胞命运的氧化还原调控：ASK1-丝裂原活化蛋白激酶途径在应激信号传导中的生理作用。
Biochim Biophys Acta. 2008 Nov;1780(11):1325-36. doi: 10.1016/j.bbagen.2007.12.011. Epub 2008 Jan 16.
8
RIP1-mediated AIP1 phosphorylation at a 14-3-3-binding site is critical for tumor necrosis factor-induced ASK1-JNK/p38 activation.RIP1介导的AIP1在14-3-3结合位点的磷酸化对于肿瘤坏死因子诱导的ASK1-JNK/p38激活至关重要。
J Biol Chem. 2007 May 18;282(20):14788-96. doi: 10.1074/jbc.M701148200. Epub 2007 Mar 27.
9
Intracellular redox regulation by the family of small GTPases.小GTP酶家族对细胞内氧化还原的调节。
Antioxid Redox Signal. 2006 Sep-Oct;8(9-10):1857-63. doi: 10.1089/ars.2006.8.1857.
10
Oxidative phosphorylation and aging.氧化磷酸化与衰老
Ageing Res Rev. 2006 Nov;5(4):402-33. doi: 10.1016/j.arr.2006.04.001. Epub 2006 Jul 10.
Zotero 插件