ArticleProceedings of the American Thoracic Society2011
Proteostasis: a new therapeutic paradigm for pulmonary disease.
Article in Proceedings of the American Thoracic Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 45 citations in OpenAlex.
- The role of sleep disorders in orchestrating proteomic dysfunction and multi-morbidity.Molecular psychiatry · 2026Review
- Novel Gene Therapy Approaches for Targeting Neurodegenerative Disorders: Focusing on Delivering Neurotrophic Genes.Molecular neurobiology · 2025Review
- Lung Single-Cell Transcriptomics Offers Insights into the Pulmonary Interstitial Toxicity Caused by Silica Nanoparticles.Environment & health (Washington, D.C.) · 2024Article
- Article
- Activation of immune cell proteasomes in peripheral blood of smokers and COPD patients: implications for therapy.The European respiratory journal · 2022Article
- Anakinra restores cellular proteostasis by coupling mitochondrial redox balance to autophagy.The Journal of clinical investigation · 2022Article
- The heat shock response and small molecule regulators.European journal of medicinal chemistry · 2021Review
- The Autophagy Pathway: A Critical Route in the Disposal of Alpha 1-Antitrypsin Aggregates That Holds Many Mysteries.International journal of molecular sciences · 2021Review
- The Critical Roles of Proteostasis and Endoplasmic Reticulum Stress in Atrial Fibrillation.Frontiers in physiology · 2021Review
- Correction of Niemann-Pick type C1 trafficking and activity with the histone deacetylase inhibitor valproic acid.The Journal of biological chemistry · 2020Article
- Alpha 1-Antitrypsin Deficiency: A Disorder of Proteostasis-Mediated Protein Folding and Trafficking Pathways.International journal of molecular sciences · 2020Review
- Ubiquitin-proteasome signaling in lung injury.Translational research : the journal of laboratory and clinical medicine · 2018Review
- A systematic atlas of chaperome deregulation topologies across the human cancer landscape.PLoS computational biology · 2018Article
- SCFThe Journal of biological chemistry · 2017Article
- Measuring the Effect of Histone Deacetylase Inhibitors (HDACi) on the Secretion and Activity of Alpha-1 Antitrypsin.Methods in molecular biology (Clifton, N.J.) · 2017Article
- Blue journal conference. Aging and susceptibility to lung disease.American journal of respiratory and critical care medicine · 2015Review
- Proteostasis in pediatric pulmonary pathology.Molecular and cellular pediatrics · 2014Article
- Malfolded protein structure and proteostasis in lung diseases.American journal of respiratory and critical care medicine · 2014Article
- The emerging role of the ubiquitin proteasome in pulmonary biology and disease.American journal of respiratory and critical care medicine · 2013Review
- Histone deacetylase inhibitor (HDACi) suberoylanilide hydroxamic acid (SAHA)-mediated correction of α1-antitrypsin deficiency.The Journal of biological chemistry · 2012Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 3 countries.
Funding
Abstract
Among lung pathologies, α1AT, chronic obstructive pulmonary disease (COPD), emphysema, and asthma are diseases triggered by local environmental stress in the airway that we refer to herein collectively as airway stress diseases (ASDs). A deficiency of α-1-antitrypsin (α1AT) is an inherited genetic disorder that is a consequence of the misfolding of α1AT during protein synthesis in liver hepatocytes, reducing secretion to the plasma and delivery to the lung. Deficiency of α1AT in the lung triggers a similar pathological phenotype to other ASDs. Moreover, the loss of α1AT in the lung is a well-known environmental risk factor for COPD/emphysema. To date there are no effective therapeutic approaches to address ASDs, which reflects a general lack of understanding of their cellular basis. Herein, we propose that ASDs are disorders of proteostasis. That is, they are initiated and propagated by a common theme-a challenge to protein folding capacity maintained by the proteostasis network (PN) (see Balch et al., Science 2008;319:916-919). The PN is a network of chaperones and degradative components that generates and manages protein folding pathways responsible for normal human physiology. In ASD, we suggest that the PN system fails to respond to the increased burden of unfolded proteins due to genetic and environmental stresses, thus triggering pulmonary pathophysiology. We introduce the enabling concept of proteostasis regulators (PRs), small molecules that regulate signaling pathways that control the composition and activity of PN components, as a new and general approach for therapeutic management of ASDs.
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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.