ArticleCell death and differentiation2017
Autophagy induced by DAMPs facilitates the inflammation response in lungs undergoing ischemia-reperfusion injury through promoting TRAF6 ubiquitination.
Article in Cell death and differentiation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
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Who cites it
74 citing papers in PubMed, 106 citations in OpenAlex.
- Small-molecule autophagy modulators: Mechanisms, therapeutic potential, and development challenges in pathological settings.Fundamental research · 2026Review
- Dynamic regulation and targeted intervention of neutrophils in hepatic ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2026Review
- Autophagy-Neuroinflammation Axis in Neurodegenerative Diseases: Mechanisms and Therapeutic Potential.Cells · 2026Review
- TRAF6, a gga-miR-7b Target, PromotesBiomolecules · 2026Article
- Relationship between different modes of death and premature ovarian insufficiency: a literature review.Apoptosis : an international journal on programmed cell death · 2026Review
- Macrophage polarization in ischemia-reperfusion injury: from molecular mechanisms to therapeutic strategies.Frontiers in immunology · 2026Review
- NEDD4 suppresses ferroptosis in lung ischemia-reperfusion injury by ubiquitinating and degrading SLC1A5.Scientific reports · 2025Article
- Carbon Monoxide as a Molecular Modulator of Ischemia-Reperfusion Injury: New Insights for Translational Application in Organ Transplantation.International journal of molecular sciences · 2025Review
- mTOR and autophagy in acute lung injury pathogenesis and therapeutic potential.Journal of thoracic disease · 2025Review
- HMGB1 in Septic Muscle Atrophy: Roles and Therapeutic Potential for Muscle Atrophy and Regeneration.Journal of cachexia, sarcopenia and muscle · 2025Review
- Spatial transcriptomics reveals distinct role of monocytes/macrophages with highFrontiers in immunology · 2025Article
- Deoxypodophyllotoxin Mediates Autophagy Death through Inhibition of GRP78 in Human Osteosarcoma.Current cancer drug targets · 2025Article
- Impact of Pre-Transplant Left Ventricular Diastolic Pressure on Primary Graft Dysfunction after Lung Transplantation: A Narrative Review.Diagnostics (Basel, Switzerland) · 2024Review
- The protective effect of carbamazepine on acute lung injury induced by hemorrhagic shock and resuscitation in rats.PloS one · 2024Article
- Regulated Cell Death of Alveolar Macrophages in Acute Lung Inflammation: Current Knowledge and Perspectives.Journal of inflammation research · 2024Review
- Hemopexin alleviates sterile inflammation in ischemia-reperfusion-induced lung injury.Frontiers in immunology · 2024Article
- Ischemic postconditioning protects against acute kidney injury after limb ischemia reperfusion by regulating HMGB1 release and autophagy.Renal failure · 2023Article
- TRAF6 triggers Mycobacterium-infected host autophagy through Rab7 ubiquitination.Cell death discovery · 2023Article
- VEGFC ameliorates salt-sensitive hypertension and hypertensive nephropathy by inhibiting NLRP3 inflammasome via activating VEGFR3-AMPK dependent autophagy pathway.Cellular and molecular life sciences : CMLS · 2023Article
- The interaction between autophagy, Helicobacter pylori, and gut microbiota in gastric carcinogenesis.Trends in microbiology · 2023Review
14 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lung ischemia-reperfusion (I/R) injury remains one of the most common complications after various cardiopulmonary surgeries. The inflammation response triggered by the released damage-associated molecular patterns (DAMPs) aggravates lung tissue damage. However, little is known about the role of autophagy in the pathogenesis of lung I/R injury. Here, we report that a variety of inflammation-related and autophagy-associated genes are rapidly upregulated, which facilitate the inflammation response in a minipig lung I/R injury model. Left lung I/R injury triggered inflammatory cytokine production and activated the autophagy flux as evidenced in crude lung tissues and alveolar macrophages. This was associated with the release of DAMPs, such as high mobility group protein B1 (HMGB1) and heat shock protein 60 (HSP60). Indeed, treatment with recombinant HMGB1 or HSP60 induced autophagy in alveolar macrophages, whereas autophagy inhibition by knockdown of ATG7 or BECN1 markedly reduced DAMP-triggered production of inflammatory cytokines including IL-1β, TNF and IL12 in alveolar macrophages. This appeared to be because of decreased activation of MAPK and NF-κB signaling. Furthermore, knockdown of ATG7 or BECN1 inhibited Lys63 (K63)-linked ubiquitination of TNF receptor-associated factor 6 (TRAF6) in DAMP-treated alveolar macrophages. Consistently, treatment with 3-MA inhibited K63-linked ubiquitination of TRAF6 in I/R-injured lung tissues in vivo. Collectively, these results indicate that autophagy triggered by DAMPs during lung I/R injury amplifies the inflammatory response through enhancing K63-linked ubiquitination of TRAF6 and activation of the downstream MAPK and NF-κB signaling.
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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.