title: Differential regulation of autophagy and mitophagy in pulmonary diseases.
abstract: 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.
authors.affiliation: Division of Molecular and Translational Biomedicine, Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham School of Medicine, Birmingham, Alabama;
authors.forename: Saurabh
authors.initials: S
authors.lastname: Aggarwal
authors.affiliation: Department of Pulmonary, Critical Care and Sleep Medicine, Yale University School of Medicine, New Haven, Connecticut; and.
authors.forename: Praveen
authors.initials: P
authors.lastname: Mannam
authors.affiliation: Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama jianhuazhang@uabmc.edu.
authors.forename: Jianhua
authors.initials: J
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001343:Autophagy; D006801:Humans; D008171:Lung Diseases / Q000473:pathology*; D008247:Lysosomes / Q000502:physiology; D008928:Mitochondria / Q000502:physiology; D063306:Mitophagy; D015398:Signal Transduction
keywords: ALI; COPD; IPF; PAH; PH