The Role of Mitochondrial DNA in Mediating Alveolar Epithelial Cell Apoptosis and Pulmonary Fibrosis

被引：120

作者：

Kim, Seok-Jo ^{[1
,2
]}

Cheresh, Paul ^{[1
,2
]}

Jablonski, Renea P. ^{[1
,2
]}

Williams, David B. ^{[1
,2
]}

Kamp, David W. ^{[1
,2
]}

机构：

[1] Jesse Brown VA Med Ctr, Div Pulm & Crit Care Med, Dept Med, Chicago, IL 60612 USA

[2] Northwestern Univ, Feinberg Sch Med, Div Pulm & Crit Care Med, Chicago, IL 60611 USA

来源：

INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2015年 / 16卷 / 09期

关键词：

mitochondrial DNA damage; oxidative stress; Sirtuin; 3; alveolar epithelial cell; pulmonary fibrosis; PLASMINOGEN-ACTIVATOR INHIBITOR-1; GLYCOSYLASE; PROTECTS; INDUCED LUNG INJURY; KINASE-C-DELTA; OXIDATIVE STRESS; REACTIVE OXYGEN; GENE-EXPRESSION; EXTRACELLULAR-MATRIX; CALORIC RESTRICTION; HYDROGEN-PEROXIDE;

D O I：

10.3390/ijms160921486

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

Convincing evidence has emerged demonstrating that impairment of mitochondrial function is critically important in regulating alveolar epithelial cell (AEC) programmed cell death (apoptosis) that may contribute to aging-related lung diseases, such as idiopathic pulmonary fibrosis (IPF) and asbestosis (pulmonary fibrosis following asbestos exposure). The mammalian mitochondrial DNA (mtDNA) encodes for 13 proteins, including several essential for oxidative phosphorylation. We review the evidence implicating that oxidative stress-induced mtDNA damage promotes AEC apoptosis and pulmonary fibrosis. We focus on the emerging role for AEC mtDNA damage repair by 8-oxoguanine DNA glycosylase (OGG1) and mitochondrial aconitase (ACO-2) in maintaining mtDNA integrity which is important in preventing AEC apoptosis and asbestos-induced pulmonary fibrosis in a murine model. We then review recent studies linking the sirtuin (SIRT) family members, especially SIRT3, to mitochondrial integrity and mtDNA damage repair and aging. We present a conceptual model of how SIRTs modulate reactive oxygen species (ROS)-driven mitochondrial metabolism that may be important for their tumor suppressor function. The emerging insights into the pathobiology underlying AEC mtDNA damage and apoptosis is suggesting novel therapeutic targets that may prove useful for the management of age-related diseases, including pulmonary fibrosis and lung cancer.

引用

页码：21486 / 21519

页数：34

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