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热休克蛋白可以保护衰老的人类和啮齿动物细胞免受不同应激刺激。

Heat shock proteins can protect aged human and rodent cells from different stressful stimuli.

作者信息

Alsbury Sam, Papageorgiou Konstantina, Latchman David S

机构信息

Medical Molecular Biology Unit, Institute of Child Health, UCL, 30 Guilford Street, London WC1N 7HX, UK.

出版信息

Mech Ageing Dev. 2004 Mar;125(3):201-9. doi: 10.1016/j.mad.2003.11.015.

Abstract

Heat shock proteins (hsps) are induced by stressful stimuli and have been shown to protect cells and organs from such stresses both in vitro and in vivo. Because of this, mildly stressful stimuli, sufficient to induce hsp over-expression can protect against a subsequent more severe stress. In cells from aged individuals, however, no hsp induction is observed upon exposure to stress and no protective effect of a mild stress is observed. Here, we show that bypassing the block to hsp induction by artificially over-expressing hsps, can produce a protective effect against a variety of damaging stimuli in cells from aged rats or aged humans, indicating that hsps can have a protective effect in aged cells, provided successful over-expression can be achieved. Hence, hsps over-expression could be of therapeutic benefit in aged individuals if procedures to over-express the hsps can be developed either by devising non-stressful procedures to induce endogenous hsp over-expression or by developing vectors able to efficiently deliver exogenous hsps.

摘要

热休克蛋白(hsps)由应激刺激诱导产生,并且已证实在体外和体内均可保护细胞和器官免受此类应激影响。正因如此,足以诱导hsp过度表达的轻度应激刺激可预防随后更严重的应激。然而,在老年个体的细胞中,应激时未观察到hsp诱导,轻度应激也未产生保护作用。在此,我们表明,通过人工过度表达hsp绕过hsp诱导障碍,可对老年大鼠或老年人类细胞中的多种损伤刺激产生保护作用,这表明只要能成功实现过度表达,hsp在老年细胞中就可发挥保护作用。因此,如果能够通过设计非应激程序诱导内源性hsp过度表达或开发能够有效递送外源性hsp的载体来制定hsp过度表达的程序,那么hsp过度表达可能对老年个体具有治疗益处。

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