Jäättelä M
Apoptosis Laboratory, Institute of Cancer Biology, Danish Cancer Society, Copenhagen.
Ann Med. 1999 Aug;31(4):261-71. doi: 10.3109/07853899908995889.
Cells have developed complex ways to respond to various stresses. Interestingly, stresses such as heat, ischaemia and radiation can induce different cellular responses depending on their strength. While a mild stress induces a protective heat shock response, a more potent stress stimulus induces apoptosis and an even stronger one leads to necrosis. The heat shock or stress response, ie the synthesis of heat shock proteins (Hsps, stress proteins) in response to a mild stress, allows cells to adapt to gradual changes in their environment and to survive in otherwise lethal conditions. The ability of Hsps to protect cultured cells from both apoptosis and necrosis has been well demonstrated. Novel data suggest an important protective role for them also in vivo as they can protect heart and brain against ischaemia and lungs and liver against sepsis. Moreover, they can render tumours resistant to anticancer therapy. These and other cytoprotective effects of Hsps make them tempting targets for therapeutic interventions in several diseases.
细胞已形成复杂的方式来应对各种应激。有趣的是，诸如热、缺血和辐射等应激根据其强度可诱导不同的细胞反应。轻度应激会诱导保护性热休克反应，而更强的应激刺激则会诱导细胞凋亡，更强的应激会导致坏死。热休克或应激反应，即细胞在轻度应激下合成热休克蛋白（Hsps，应激蛋白），使细胞能够适应环境的逐渐变化，并在原本致命的条件下存活。Hsps保护培养细胞免于凋亡和坏死的能力已得到充分证明。新数据表明它们在体内也具有重要的保护作用，因为它们可以保护心脏和大脑免受缺血影响，保护肺和肝脏免受败血症影响。此外，它们可使肿瘤对抗癌治疗产生抗性。Hsps的这些及其他细胞保护作用使其成为多种疾病治疗干预的诱人靶点。
