热休克因子 1 (HSF1) 和热休克蛋白 (HSP) 在铁死亡中的新作用。,Pathophysiology

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热休克因子 1 (HSF1) 和热休克蛋白 (HSP) 在铁死亡中的新作用。
Pathophysiology Pub Date : 2023-03-14 , DOI: 10.3390/pathophysiology30010007
Iman Aolymat ₁ , Ma'mon M Hatmal ₂ , Amin N Olaimat ₃

Affiliation

细胞采用一种保存完好的生理应激反应机制，称为热休克反应，以激活某种类型的分子伴侣，称为热休克蛋白 (HSP)。HSP 被称为热休克因子 (HSF) 的热休克基因的转录激活因子激活。这些分子伴侣被归类为 HSP70 超家族，其中包括 HSPA (HSP70) 和 HSPH (HSP110) 家族；DNAJ (HSP40) 家族；HSPB 家族（小型热休克蛋白 (sHSP)）；伴侣蛋白和伴侣蛋白样蛋白；和其他热诱导蛋白家族。HSP 在维持蛋白质稳态和保护细胞免受压力刺激方面起着关键作用。HSP 参与折叠新合成的蛋白质，将折叠的蛋白质保持在其天然构象中，防止蛋白质错误折叠和积累，和降解变性蛋白质。Ferroptosis 是最近发现的氧化铁依赖性细胞死亡类型。它是 Stockwell 实验室成员最近在 2012 年创造的，他们描述了一种由 erastin 或 RSL3 诱导的特殊细胞死亡。铁死亡的特征是铁积累、氧化应激增加和脂质过氧化引起的氧化状态改变，这些改变由酶促和非酶促途径介导。铁死亡细胞死亡的过程受到多重调控，涉及多种病理生理条件。近年来出现了许多研究，证明 HSP 及其调节剂热休克因子 1 (HSF1) 参与铁死亡调节。了解在铁死亡中控制 HSF1 和 HSP 的机制可用于开发针对许多病理条件下铁死亡发生的治疗干预措施。因此，本综述全面总结了铁死亡的基本特征以及HSF1和HSP在铁死亡中的调控功能。

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The Emerging Role of Heat Shock Factor 1 (HSF1) and Heat Shock Proteins (HSPs) in Ferroptosis.

Cells employ a well-preserved physiological stress response mechanism, termed the heat shock response, to activate a certain type of molecular chaperone called heat shock proteins (HSPs). HSPs are activated by transcriptional activators of heat shock genes known as heat shock factors (HSFs). These molecular chaperones are categorized as the HSP70 superfamily, which includes HSPA (HSP70) and HSPH (HSP110) families; the DNAJ (HSP40) family; the HSPB family (small heat shock proteins (sHSPs)); chaperonins and chaperonin-like proteins; and other heat-inducible protein families. HSPs play a critical role in sustaining proteostasis and protecting cells against stressful stimuli. HSPs participate in folding newly synthesized proteins, holding folded proteins in their native conformation, preventing protein misfolding and accumulation, and degrading denatured proteins. Ferroptosis is a recently identified type of oxidative iron-dependent cell demise. It was coined recently in 2012 by Stockwell Lab members, who described a special kind of cell death induced by erastin or RSL3. Ferroptosis is characterized by alterations in oxidative status resulting from iron accumulation, increased oxidative stress, and lipid peroxidation, which are mediated by enzymatic and non-enzymatic pathways. The process of ferroptotic cell death is regulated at multiple, and it is involved in several pathophysiological conditions. Much research has emerged in recent years demonstrating the involvement of HSPs and their regulator heat shock factor 1 (HSF1) in ferroptosis regulation. Understanding the machinery controlling HSF1 and HSPs in ferroptosis can be employed in developing therapeutic interventions for ferroptosis occurrence in a number of pathological conditions. Therefore, this review comprehensively summarized the basic characteristics of ferroptosis and the regulatory functions of HSF1 and HSPs in ferroptosis.

更新日期：2023-03-14

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