Differential regulation of autophagy and mitophagy in pulmonary diseases

被引:119
作者
Aggarwal, Saurabh [1 ]
Mannam, Praveen [2 ]
Zhang, Jianhua [3 ]
机构
[1] Univ Alabama Birmingham, Med Sch Birmingham, Dept Anesthesiol & Perioperat Med, Div Mol & Translat Biomed, Birmingham, AL USA
[2] Yale Univ, Sch Med, Dept Pulm Crit Care & Sleep Med, New Haven, CT USA
[3] Univ Alabama Birmingham, Dept Pathol, Birmingham, AL USA
关键词
ALI; COPD; IPF; PAH; PH; ENDOPLASMIC-RETICULUM STRESS; ENDOTHELIAL-CELL DEATH; LUNG EPITHELIAL-CELLS; NF-KAPPA-B; SELECTIVE AUTOPHAGY; UP-REGULATION; MITOCHONDRIAL DYSFUNCTION; INSUFFICIENT AUTOPHAGY; INFLAMMATORY RESPONSES; ARTERIAL-HYPERTENSION;
D O I
10.1152/ajplung.00128.2016
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Lysosomal-mediated degradation of intracellular lipids, proteins and organelles, known as autophagy, represents a inducible adaptive response to lung injury resulting from exposure to insults, such as hypoxia, microbes, inflammation, ischemia-reperfusion, pharmaceuticals (e.g., bleomycin), or inhaled xenobiotics (i.e., air pollution, cigarette smoke). This process clears damaged or toxic cellular constituents and facilitates cell survival in stressful environments. Autophagic degradation of dysfunctional or damaged mitochondria is termed mitophagy. Enhanced mitophagy is usually an early response to promote survival. However, overwhelming or prolonged mitochondrial damage can induce excessive/pathological levels of mitophagy, thereby promoting cell death and tissue injury. Autophagy/mitophagy is therefore an important modulator in human pulmonary diseases and a potential therapeutic target. This review article will summarize the most recent studies highlighting the role of autophagy/mitophagy and its molecular pathways involved in stress response in pulmonary pathologies.
引用
收藏
页码:L433 / L452
页数:20
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