线粒体自噬与肺部疾病的研究进展

基础医学与临床 ›› 2020, Vol. 40 ›› Issue (6): 842-846.

线粒体自噬与肺部疾病的研究进展

谭诗旖, 陈适^*

湖南师范大学医学院, 湖南长沙 410006

收稿日期:2019-12-05 修回日期:2020-03-21 出版日期:2020-06-05 发布日期:2020-05-29
通讯作者: *chenshonest@163.com
基金资助:
国家自然科学基金(81703199);湖南省教育厅一般项目(16C0958)

Progress in research on mitophagy and pulmonary diseases

TAN Shi-Yi, CHEN Shi^*

School of Medicine,Hunan Normal University,Changsha 410006,China

Received:2019-12-05 Revised:2020-03-21 Online:2020-06-05 Published:2020-05-29
Contact: *chenshonest@163.com

摘要/Abstract

摘要： 线粒体自噬是选择性自噬的重要形式之一,可通过调控生物体内线粒体质量影响肺部疾病发生发展。线粒体自噬在不同的肺部疾病中发挥着不同的作用。如在特发性肺纤维化与急性肺损伤中,线粒体自噬水平过高或过低都可加重病情;而在肺动脉高压中,线粒体自噬水平过高时会产生损害效应。除此之外,在慢性阻塞性肺疾病中,线粒体自噬可调节细胞坏死以及控制细胞炎性反应。因此,深入了解线粒体自噬调控机制对肺部疾病的防治具有重要意义。

关键词: 线粒体功能障碍, 线粒体自噬, 肺部疾病

Abstract: Mitophagy is one of the important forms of selective autophagy, which affects the occurrence and development of lung diseases by regulating the quality of mitochondria in vivo. Mitophagy has different functions in different lung diseases. In idiopathic pulmonary fibrosis and acute lung injury, excessive or low levels of mitophagy can aggravate the diseases; while in pulmonary hypertension, excessive mitophagy levels play the adverse effect in the progress of the disease. Additionally, in chronic obstructive pulmonary disease, mitophagy can regulate cell necrosis and control cellular inflammation. Therefore, it is important to understand the mechanism of mitophagy to prevent and treat lung diseases.

Key words: mitochondrial dysfunction, mitophagy, lung disease

中图分类号:

R364

谭诗旖, 陈适. 线粒体自噬与肺部疾病的研究进展[J]. 基础医学与临床, 2020, 40(6): 842-846.

TAN Shi-Yi, CHEN Shi. Progress in research on mitophagy and pulmonary diseases[J]. Basic & Clinical Medicine, 2020, 40(6): 842-846.

参考文献

[1]Ryter SW, Rosas IO, Owen CA, et al. Mitochondrial dysfunction as a pathogenic mediator of chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis[J]. Ann Am Thorac Soc, 2018, 15: S266-S272.
[2]Yamashita SI, Kanki T. How autophagy eats large mitochondria: autophagosome formation coupled with mitochondrial fragmentation[J]. Autophagy, 2017, 13: 980-981.
[3]Cummins N, Götz J. Shedding light on mitophagy in neurons: what is the evidence for PINK1/PARKIN mitophagy in vivo[J]. Cell Mol Life Sci, 2018, 75:1151-1162.
[4]Durcan TM, Fon EA. The three ‘P’ s of mitophagy: PARKIN, PINK1, and post-translational modifications[J]. Genes Dev, 2015, 29: 989-999.
[5]Rodger CE, McWilliams TG, Ganley IG. Mammalian mitophagy-from in vitro molecules to in vivo models[J]. FEBS J, 2018, 285: 1185-1202.
[6]Heukels P, Moor CC, von der Thüsen JH, et al. Inflammation and immunity in IPF pathogenesis and treatment[J]. Respir Med, 2019, 147: 79-91.
[7]Mora AL, Bueno M, Rojas M. Mitochondria in the spotlight of aging and idiopathic pulmonary fibrosis[J]. J Clin Invest, 2017, 127: 405-414.
[8]Siani A, Tirelli N. Myofibroblast differentiation: main features, biomedical relevance, and the role of reactive oxygen species[J]. Antioxid Redox Signal, 2014, 21: 768-785.
[9]Zank DC, Bueno M, Mora AL, et al. Idiopathic pulmon-ary fibrosis: aging, mitochondrial dysfunction, and cellular bioenergetics[J]. Front Med (Lausanne), 2018, 5: 10. doi: 10.3389/fmed.2018.00010.
[10]Larson-Casey JL, Deshane JS, Ryan AJ, et al. Macro-phage Akt1 kinase-mediated mitophagy modulates apoptosis resistance and pulmonary fibrosis[J]. Immunity, 2016, 44: 582-596.
[11]Jiang S, Sun J, Mohammadtursun N, et al. Dual role of autophagy/mitophagy in chronic obstructive pulmonary disease[J]. Pulm Pharmacol Ther, 2019, 56: 116-125.
[12]Even B, Fayad-Kobeissi S, Gagliolo JM, et al. Heme oxygenase-1 induction attenuates senescence in chronic obstructive pulmonary disease lung fibroblasts by protecting against mitochondria dysfunction[J]. Aging Cell, 2018, 17: e12837. doi: 10.1111/acel.12837.
[13]Barnes PJ. Pulmonary diseases and ageing[J]. Subcell Biochem, 2019, 91: 45-74.
[14]Jiang Y, Wang X, Hu D. Mitochondrial alterations during oxidative stress in chronic obstructive pulmonary disease[J]. Int J Chron Obstruct Pulmon Dis, 2017, 12: 1153-1162.
[15]Mercado N, Ito K, Barnes PJ. Accelerated ageing of the lung in COPD: new concepts[J].Thorax, 2015, 70: 482-489.
[16]Ito S, Araya J, Kurita Y, et al. PARK2-mediated mitophagy is involved in regulation of HBEC senescence in COPD pathogenesis[J]. Autophagy, 2015, 11: 547-559.
[17]Hoeper MM, Ghofrani HA, Grünig E, et al. Pulmonary hypertension[J]. Dtsch Arztebl Int, 2017, 114: 73-84.
[18]Husain-Syed F, Birk HW, Tello K, et al. Alterations in Doppler-derived renal venous stasis index during recompensation of right heart failure and fluid overload in a patient with pulmonary hypertension[J]. Rev Cardiovasc Med, 2019, 20: 263-266.
[19]Yu Q, Chan SY. Mitochondrial and metabolic drivers of pulmonary vascular endothelial dysfunction in pulmonary hypertension[J]. Adv Exp Med Biol, 2017, 967: 373-383.
[20]Tahrir FG, Langford D, Amini S, et al. Mitochondrial quality control in cardiac cells: mechanisms and role in cardiac cell injury and disease[J]. J Cell Physiol, 2019, 234: 8122-8123.
[21]Marshall JD, Bazan I, Zhang Y, et al. Mitochondrial dysfunction and pulmonary hypertension: cause, effect, or both[J]. Am J Physiol Lung Cell Mol Physiol, 2018, 314: L782-L796.
[22]Liu J, Du J, Cheng X, et al. Effect of Netrin-1 anti-inflammatory factor on acute lung injury in Sepsis rats[J]. Med Sci Monit, 2019, 25: 7928-7935.
[23]Mannam P, Shinn AS, Srivastava A, et al. MKK3 regulates mitochondrial biogenesis and mitophagy in sepsis-induced lung injury[J]. Am J Physiol Lung Cell Mol Physiol, 2014, 306: L604-L619.
[24]Um JH, Yun J. Emerging role of mitophagy in human diseases and physiology[J]. BMB Rep, 2017, 50: 299-307.
[25]Zhang Y, Sauler M, Shinn AS, et al. Endothelial PINK1 mediates the protective effects of NLRP3 deficiency during lethal oxidant injury[J]. J Immunol, 2014, 192: 5296-5304.
[26]Simon HU, Friis R, Tait SWG, et al. Retrograde signal-ing from autophagy modulates stress responses[J]. Sci Signal, 2017, 10: e2791. doi: 10.1126/scisignal.aag2791.
[27]Chen S, Yuan J, Yao S, et al. Lipopolysaccharides may aggravate apoptosis through accumulation of autophago-somes in alveolar macrophages of human silicosis[J]. Autophagy, 2015, 11: 2346-2357.
[28]He X, Chen S, Li C, et al. Trehalose alleviates crystalline silica-induced pulmonary fibrosis via activation of the TFEB-mediated autophagy-lysosomal system in alveolar macrophages[J]. Cells, 2020, 9: 122-142.