ReviewAnnals of the American Thoracic Society2016
Autophagy: Friend or Foe in Lung Disease?
Review in Annals of the American Thoracic Society, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 84 citations in OpenAlex.
- Salvianolic Acid A Relieves Acute Lung Injury by Promoting the Expression of FOXO1 and Activating Autophagy Through the Inhibition of miR-217-5p.Biochemical genetics · 2026Article
- Integrated transcriptomic and metabolomic profiling reveals immune-metabolic crosstalk and predictive biomarkers of ligustrazine treatment response in idiopathic pulmonary fibrosis.Journal of translational medicine · 2026Article
- When Autophagy Fails:American journal of respiratory cell and molecular biology · 2025Article
- Nutrition, Lifestyle, and Environmental Factors in Lung Homeostasis and Respiratory Health.Nutrients · 2025Review
- A comprehensive review on the cellular mechanism of traditional Chinese medicine in the treatment of pediatric lung diseases.BioImpacts : BI · 2025Review
- Understanding the autophagic functions in cancer stem cell maintenance and therapy resistance.Expert reviews in molecular medicine · 2024Review
- Cellular and molecular mechanisms of cell damage and cell death in ischemia-reperfusion injury in organ transplantation.Molecular biology reports · 2024Review
- A systematic review of the research progress of traditional Chinese medicine against pulmonary fibrosis: from a pharmacological perspective.Chinese medicine · 2023Review
- Airway Epithelium Senescence as a Driving Mechanism in COPD Pathogenesis.Biomedicines · 2023Review
- cAMP-PDE signaling in COPD: Review of cellular, molecular and clinical features.Biochemistry and biophysics reports · 2023Review
- The inhibitory effect of quercetin-3-glucuronide on pulmonary injury in vitro and in vivo.Journal of food and drug analysis · 2023Article
- Role of heparanase in pulmonary hypertension.Frontiers in pharmacology · 2023Review
- Article
- Endolysosomal Cation Channels and Lung Disease.Cells · 2022Review
- Lung emphysema and impaired macrophage elastase clearance in mucolipin 3 deficient mice.Nature communications · 2022Article
- Role and Mechanism of Keap1/Nrf2 Signaling Pathway in the Regulation of Autophagy in Alleviating Pulmonary Fibrosis.Computational intelligence and neuroscience · 2022Article
- Secretory Autophagosomes from Alveolar Macrophages Exacerbate Acute Respiratory Distress Syndrome by Releasing IL-1β.Journal of inflammation research · 2022Article
- Investigation of the role of the autophagic protein LC3B in the regulation of human airway epithelium cell differentiation in COPD using a biomimetic model.Materials today. Bio · 2022Article
- Article
- Role of chaperone-mediated autophagy in the pathophysiology including pulmonary disorders.Inflammation and regeneration · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Autophagy is a highly conserved process by which cells can recycle organelles and proteins by degrading them in the lysosomes. Although autophagy is considered a dynamic system responsible for cellular renovation and homeostasis under physiological conditions, it is increasingly clear that autophagy is directly relevant to clinical disease. During disease progression, autophagy not only serves as a cellular protective mechanism but also can represent a harmful event under certain conditions. In addition, although autophagy can act as a nonselective bulk degradation process, recent research shows that autophagy can selectively degrade specific proteins, organelles, and invading bacteria, in processes termed "selective autophagy." Selective autophagy has drawn the attention of researchers because of its potential importance in clinical diseases. In this article, we outline the most recent studies implicating autophagy and selective autophagy in human lung diseases, including chronic obstructive pulmonary disease, pulmonary hypertension, idiopathic pulmonary fibrosis, and sepsis. We also discuss the relationship between autophagy and other molecular mechanisms related to disease progression, including programmed necrosis (necroptosis) and the inflammasome, an inflammatory signaling platform that regulates the secretion of IL-1β and IL-18. Finally, we examine the dual nature of autophagy and selective autophagy in the lung, which have both protective and injurious effects for human lung disease.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.