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引发应激和热休克蛋白70在心肌和骨骼肌缺血再灌注损伤保护中的作用。

Role of priming stresses and Hsp70 in protection from ischemia-reperfusion injury in cardiac and skeletal muscle.

作者信息

Lepore D A, Knight K R, Anderson R L, Morrison W A

机构信息

Immunology Research Center, St Vincent's Hospital, Fitzroy, Melbourne, Victoria, Australia.

出版信息

Cell Stress Chaperones. 2001 Apr;6(2):93-6. doi: 10.1379/1466-1268(2001)006<0093:ropsah>2.0.co;2.

DOI:10.1379/1466-1268(2001)006<0093:ropsah>2.0.co;2
PMID:11599579
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC434395/
Abstract

Ischemia-reperfusion injury limits the survival of muscle involved in tissue trauma or transfers during microsurgical reconstruction. Priming stresses such as ischemic preconditioning or mild hyperthermia have frequently been associated with improved survival of ischemic-reperfused cardiac muscle, such protection coinciding with induction of the stress-related heat shock protein 70 (Hsp70). Little is known about the response of skeletal muscle to priming stresses. This review summarizes the current knowledge on the use of priming stresses as protective strategies against the consequences of ischemia-reperfusion in cardiac and skeletal muscle and the potential role of Hsp70.

摘要

缺血再灌注损伤限制了显微外科重建过程中涉及组织创伤或转移的肌肉的存活。诸如缺血预处理或轻度热疗等预处理应激常常与缺血再灌注心肌存活率的提高相关,这种保护作用与应激相关热休克蛋白70(Hsp70)的诱导相吻合。关于骨骼肌对预处理应激的反应知之甚少。本综述总结了目前关于使用预处理应激作为针对心脏和骨骼肌缺血再灌注后果的保护策略的知识以及Hsp70的潜在作用。

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本文引用的文献

1
Ischemic preconditioning: lack of delayed protection against skeletal muscle ischemia-reperfusion.
Microsurgery. 2000;20(7):350-5. doi: 10.1002/1098-2752(2000)20:7<350::aid-micr7>3.0.co;2-9.
2
Prior heat stress improves survival of ischemic-reperfused skeletal muscle in vivo.先前的热应激可提高体内缺血再灌注骨骼肌的存活率。
Muscle Nerve. 2000 Dec;23(12):1847-55. doi: 10.1002/1097-4598(200012)23:12<1847::aid-mus8>3.0.co;2-u.
3
Induction of heat-shock protein 72 in rat skeletal muscle does not increase tolerance to ischemia-reperfusion injury.大鼠骨骼肌中热休克蛋白72的诱导并不会增加对缺血再灌注损伤的耐受性。
Muscle Nerve. 1999 Mar;22(3):390-3. doi: 10.1002/(sici)1097-4598(199903)22:3<390::aid-mus12>3.0.co;2-1.
4
Whole body heat shock fails to protect mouse heart against ischemia/reperfusion injury: role of 72 kDa heat shock protein and antioxidant enzymes.全身热休克无法保护小鼠心脏免受缺血/再灌注损伤:72 kDa热休克蛋白和抗氧化酶的作用。
J Mol Cell Cardiol. 1998 Nov;30(11):2213-27. doi: 10.1006/jmcc.1998.0781.
5
Induction of 72-kDa heat shock protein does not produce second window of ischemic preconditioning in rat heart.诱导72-kDa热休克蛋白不会在大鼠心脏产生缺血预处理的第二窗口。
Am J Physiol. 1999 Jan;276(1):H224-34. doi: 10.1152/ajpheart.1999.276.1.H224.
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Stress proteins and apoptosis in prenatal development, cancer and medicine.产前发育、癌症与医学中的应激蛋白和细胞凋亡
Cell Stress Chaperones. 1998 Dec;3(4):209-12. doi: 10.1379/1466-1268(1998)003<0209:spaaip>2.3.co;2.
7
Translocation of HSP27 to cytoskeleton by repetitive hypoxia-reoxygenation in the rat myoblast cell line, H9c2.在大鼠成肌细胞系H9c2中,通过反复缺氧复氧使热休克蛋白27(HSP27)易位至细胞骨架。
Biochem Biophys Res Commun. 1998 Oct 20;251(2):576-9. doi: 10.1006/bbrc.1998.9518.
8
Whole-body hyperthermia provides biphasic cardioprotection against ischemia/reperfusion injury in the rat.全身热疗对大鼠缺血/再灌注损伤具有双相心脏保护作用。
Circulation. 1998 Oct 6;98(14):1414-21. doi: 10.1161/01.cir.98.14.1414.
9
Dissociation of heat shock proteins expression with ischemic tolerance by whole body hyperthermia in rat heart.大鼠心脏全身热疗中热休克蛋白表达与缺血耐受的解离
J Mol Cell Cardiol. 1998 Jun;30(6):1163-72. doi: 10.1006/jmcc.1998.0680.
10
Ischemic tolerance in skeletal muscle: role of nitric oxide.骨骼肌中的缺血耐受:一氧化氮的作用
Am J Physiol. 1998 Jul;275(1):H94-9. doi: 10.1152/ajpheart.1998.275.1.H94.