J Clin Invest. 2011 Aug;121(8):2972-5. doi: 10.1172/JCI59190. Epub 2011 Jul 25.
The heat shock response (HSR) is a highly conserved protective mechanism that enables cells to withstand diverse environmental stressors that disrupt protein homeostasis (proteostasis) and promote protein misfolding. It has been suggested that small-molecule drugs that elicit the HSR by activating the transcription factor heat shock factor 1 might help mitigate protein misfolding and aggregation in several devastating neurodegenerative disorders, including Huntington disease (HD). In this issue of the JCI, Labbadia et al. use a brain-penetrant Hsp90 inhibitor, HSP990, to induce the HSR in mouse models of HD. Unexpectedly, they observed that HSP990 confers only transient amelioration of a subset of HD-related phenotypes, because alterations in chromatin architecture impair the HSR upon disease progression. These findings suggest that synergistic combination therapies that simultaneously unleash the HSR and prevent its impairment are likely to be needed to restore proteostasis in HD.
热休克反应 (HSR) 是一种高度保守的保护机制,使细胞能够耐受破坏蛋白质平衡(蛋白质稳态)并促进蛋白质错误折叠的各种环境应激源。有人提出,通过激活热休克因子 1 来引发 HSR 的小分子药物可能有助于减轻几种毁灭性神经退行性疾病(包括亨廷顿病 (HD))中的蛋白质错误折叠和聚集。在本期 JCI 中,Labbadia 等人使用一种脑穿透性 HSP90 抑制剂 HSP990 诱导 HD 小鼠模型中的 HSR。出乎意料的是,他们观察到 HSP990 仅能暂时改善 HD 相关表型的一部分,因为染色质结构的改变会在疾病进展时损害 HSR。这些发现表明,可能需要协同组合疗法来同时引发 HSR 并防止其受损,以恢复 HD 中的蛋白质稳态。