ArticleAmerican journal of respiratory cell and molecular biology2009
IL-6 protects against hyperoxia-induced mitochondrial damage via Bcl-2-induced Bak interactions with mitofusins.
Article in American journal of respiratory cell and molecular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 91 citations in OpenAlex.
- Histopathological changes and inflammatory and cell death pathways in the lungs of Balb/c mice with pneumonia induced by different concentrations ofAnatomy & cell biology · 2025Article
- The Diverse Function of IL-6 in Biological Processes and the Advancement of Cancer.Immune network · 2025Review
- Bmi1 deficiency exacerbates hyperoxia-induced acute lung injury in mice.Frontiers in physiology · 2025Article
- Decoding STAT3: a new frontier in understanding and treating hyperoxic lung injury.Frontiers in immunology · 2025Review
- Interleukin 6 and cancer resistance in glioblastoma multiforme.Neurosurgical review · 2024Review
- Impact of Lysine Succinylation on the Biology of Fungi.Current issues in molecular biology · 2024Review
- Role of mitochondria in inflammatory lung diseases.Frontiers in pharmacology · 2024Review
- Role of the circulatory interleukin-6 in the pathogenesis of gliomas: A systematic review.World journal of methodology · 2022Article
- Pathophysiology and Therapy of High-Altitude Sickness: Practical Approach in Emergency and Critical Care.Journal of clinical medicine · 2022Review
- BMI1 Silencing Induces Mitochondrial Dysfunction in Lung Epithelial Cells Exposed to Hyperoxia.Frontiers in physiology · 2022Article
- A-Kinase Anchor Protein 1 deficiency causes mitochondrial dysfunction in mouse model of hyperoxia induced acute lung injury.Frontiers in pharmacology · 2022Article
- Pulmonary Interstitial Matrix and Lung Fluid Balance From Normal to the Acutely Injured Lung.Frontiers in physiology · 2021Review
- IL6-mediated HCoV-host interactome regulatory network and GO/Pathway enrichment analysis.PLoS computational biology · 2020Article
- Alda-1 Attenuates Hyperoxia-Induced Acute Lung Injury in Mice.Frontiers in pharmacology · 2020Article
- Human induced pluripotent stem cells ameliorate hyperoxia-induced lung injury in a mouse model.American journal of translational research · 2020Article
- Thiol-Redox Regulation in Lung Development and Vascular Remodeling.Antioxidants & redox signaling · 2019Review
- Alda-1 attenuates hyperoxia-induced mitochondrial dysfunction in lung vascular endothelial cells.Aging · 2019Article
- Article
- Circular RNA CircEZH2 Suppresses Transmissible Gastroenteritis Coronavirus-induced Opening of Mitochondrial Permeability Transition Pore via Targeting MiR-22 in IPEC-J2.International journal of biological sciences · 2019Article
- The role of interleukin-6-STAT3 signalling in glioblastoma.Oncology letters · 2018Review
2 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Overexpression of IL-6 markedly diminishes hyperoxic lung injury, hyperoxia-induced cell death, and DNA fragmentation, and enhances Bcl-2 expression. We hypothesized that changes in the interactions between Bcl-2 family members play an important role in the IL-6-mediated protective response to oxidative stress. Consistent with this hypothesis, we found that IL-6 induced Bcl-2 expression, both in vivo and in vitro, disrupted interactions between proapoptotic and antiapoptotic factors, and suppressed H(2)O(2)-induced loss of mitochondrial membrane potential in vitro. In addition, IL-6 overexpression in mice protects against hyperoxia-induced lung mitochondrial damage. The overexpression of Bcl-2 in vivo prolonged the survival of mice exposed to hyperoxia and inhibited alveolar capillary protein leakage. In addition, apoptosis-associated DNA fragmentation was substantially reduced in these animals. This IL-6-mediated protection was lost when Bcl-2 was silenced, demonstrating that Bcl-2 is an essential mediator of IL-6 cytoprotection. Finally, Bcl-2 blocked the dissociation of Bak from mitofusin protein (Mfn) 2, and inhibited the interaction between Bak and Mfn1. Taken together, our results suggest that IL-6 induces Bcl-2 expression to perform cytoprotective functions in response to oxygen toxicity, and that this effect is mediated by alterations in the interactions between Bak and Mfns.
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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.