ArticleJournal of molecular medicine (Berlin, Germany)2014
Defective autophagy impairs ATF3 activity and worsens lung injury during endotoxemia.
Article in Journal of molecular medicine (Berlin, Germany), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05524376 (Regulatory Network and Diagnostic Value of Key Autophagy-related Genes in Sepsis), which is not on this map. Cited by 37 papers.
What it found
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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.
Regulatory Network and Diagnostic Value of Key Autophagy-related Genes in Sepsis
Who cites it
37 citing papers in PubMed, 53 citations in OpenAlex.
- ZKSCAN3 mitigates lipopolysaccharide-induced acute lung injury by restraining excessive autophagy via activation of the mTOR pathway.Journal of thoracic disease · 2026Article
- Recombinant Human Thymosin β4 Attenuates Endotoxemia-Induced ALI and EAE by Suppressing Inflammatory and Oxidative Responses.Biomolecules · 2026Article
- A novel mechanism for treating acute lung injury with ligustilide: elucidation via network pharmacology and in vitro validation.Journal of natural medicines · 2026Article
- Novel Susceptibility Genes for Sepsis Revealed by a Cross-Tissue Transcriptome-Wide Association Study.Shock (Augusta, Ga.) · 2026Article
- ATF3 Deficiency Exacerbates Ageing-Induced Atherosclerosis and Clinical Intervention Strategy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Cell death signaling and immune regulation: new perspectives on targeted therapy for sepsis.Cellular & molecular biology letters · 2025Review
- Autophagy in Acute Lung Injury.Cell biochemistry and biophysics · 2025Review
- Tomatidine activates autophagy to improve lung injury and inflammation in sepsis by inhibiting NF-κB and MAPK pathways.Molecular genetics and genomics : MGG · 2024Article
- Activating transcription factor 3: A potential therapeutic target for inflammatory pulmonary diseases.Immunity, inflammation and disease · 2023Review
- Myeloid autophagy genes protect mice against fatal TNF- and LPS-induced cytokine storm syndromes.Autophagy · 2023Article
- Role of microRNA-494 in tumor progression.American journal of translational research · 2023Review
- TM9SF1 knockdown decreases inflammation by enhancing autophagy in a mouse model of acute lung injury.Heliyon · 2022Article
- Neuroprotective Role of α-Lipoic Acid in Iron-Overload-Mediated Toxicity and Inflammation in In Vitro and In Vivo Models.Antioxidants (Basel, Switzerland) · 2022Article
- The Role of ATF3 in Neuronal Differentiation and Development of Neuronal Networks in Opossum Postnatal Cortical Cultures.International journal of molecular sciences · 2022Article
- Dysregulation of neutrophil death in sepsis.Frontiers in immunology · 2022Review
- ATF3 induces RAB7 to govern autodegradation in paligenosis, a conserved cell plasticity program.EMBO reports · 2021Article
- Hydrogen alleviates cell damage and acute lung injury in sepsis via PINK1/Parkin-mediated mitophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Impaired autophagy increases susceptibility to endotoxin-induced chronic pancreatitis.Cell death & disease · 2020Article
- Complex interplay between autophagy and oxidative stress in the development of pulmonary disease.Redox biology · 2020Review
- Review
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledAutophagy has emerged as a key regulator of the inflammatory response. To examine the role of autophagy in the development of organ dysfunction during endotoxemia, wild-type and autophagy-deficient (Atg4b-null) mice were challenged with lipopolysaccharide. Animals lacking Atg4b showed increased mortality after endotoxemia. Among the different organs studied, only the lungs showed significant differences between genotypes, with increased damage in mutant animals. Autophagy was activated in lungs from wild-type, LPS-treated mice. Similarly, human bronchial cells show an increased autophagy when exposed to serum from septic patients. We found an increased inflammatory response (increased neutrophilic infiltration, higher levels of Il6, Il12p40, and Cxcl2) in the lungs from knockout mice and identified perinuclear sequestration of the anti-inflammatory transcription factor ATF3 as the putative mechanism responsible for the differences between genotypes. Finally, induction of autophagy by starvation before LPS exposure resulted in a dampened pulmonary response to LPS in wild-type, but not knockout, mice. Similar results were found in human bronchial cells exposed to LPS. Our results demonstrate the central role of autophagy in the regulation of the lung response to endotoxemia and sepsis and its potential modulation by nutrition. KEY MESSAGES: Endotoxemia and sepsis trigger autophagy in lung tissue. Defective autophagy increases mortality and lung inflammation after endotoxemia. Impairment of autophagy results is perinuclear ATF3 sequestration. Starvation ameliorates lung injury by an autophagy-dependent mechanism.
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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.