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Cathepsin L与线粒体自噬(2)

     6.结论

    受损的线粒体可通过线粒体自噬被清除以保证细胞内线粒体的质量,维持细胞稳态。线粒体自噬受各种调控分子的精细调节,包括DJ-1、PINK1和Parkin 等自噬蛋白,而Cathepsin L和自噬蛋白之间通过Ca2+加以联系。线粒体自噬的异常与神经退行性疾病如PD等密切相关。但是,还需要更多的细节和量化的研究来探究Cathepsin L在线粒体自噬中的作用。随着对线粒体自噬研究的深入,可能为PD等神经退行性疾病提供新的治疗靶点。

    参考文献:

    [1]Boya P and Kroemer G. Lysosomal membrane permeabilization in cell death. Oncogene, 2008. 27:6434-6451.

    [2]Amuthan G, Biswas G, Zhang SY, et al. Mitochondria-to-nucleus stress signaling induces phenotypic changes, tumor progression and cell invasion. EMBO J, 2001. 20:1910-1920.

    [3]Lemasters JJ. Selective mitochondrial autophagy, or mitophagy, as a targeted defense against oxidative stress, mitochondrial dysfunction, and aging. Rejuvenation Res, 2005. 8:3-5.

    [4]Gao H, Yang W, Qi Z, et al. DJ-1 protects dopaminergic neurons against rotenone-induced apoptosis by enhancing ERK-dependent mitophagy. J Mol Biol, 2012. 423:232-248.

    [5]Narendra D, Tanaka A, Suen DF, et al. Parkin is recruited selectively to impaired mitochondria and promotes their autophagy. J Cell Biol, 2008. 183:795-803.

    [6]Shtifman A, Zhong N, Lopez JR, et al. Altered Ca2+ homeostasis in the skeletal muscle of DJ-1 null mice. Neurobiol Aging, 2011. 32:125-132.

    作者簡介:

    徐舒青,女,硕士,药师,研究方向:临床药学。, 百拇医药
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