ArticleRespiratory research2023
AMPK activation improves recovery from pneumonia-induced lung injury via reduction of er-stress and apoptosis in alveolar epithelial cells.
Article in Respiratory research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 25 citations in OpenAlex.
- Mitochondrial-endoplasmic reticulum interactions in lung diseases.Cell death & disease · 2026Review
- Gymnemagenin-3-O-glucuronide mitigates lipopolysaccharide-induced acute lung inflammation/injury by regulating the NF-κB/MAPK signalling.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Sbno2-mediated tissue-resident alveolar macrophages: a novel therapeutic axis for sepsis-induced acute lung injury.Cell death discovery · 2026Review
- Altered Metabolism in Idiopathic Pulmonary Fibrosis.Journal of cellular physiology · 2025Review
- Kaempferol MitigatesPharmaceuticals (Basel, Switzerland) · 2025Article
- Cell Death and Infection: Implications for Host and Microbe.Advances in experimental medicine and biology · 2025Review
- Iron Overload-induced Ferroptosis as a Target for Protection against Obliterative Bronchiolitis after Orthotopic Tracheal Transplantation in Mice.Current molecular medicine · 2025Article
- Alveolar epithelial cells in bacterial sepsis-associated acute lung injury: mechanisms and therapeutic strategies.Frontiers in immunology · 2025Review
- Cross-talk between aging resilience pathways and autoimmunity onset.Frontiers in immunology · 2025Review
- Myeloid Cell-Specific Deletion of AMPKα1 Worsens Ocular Bacterial Infection by Skewing Macrophage Phenotypes.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- J147 treatment protects against traumatic brain injury by inhibiting neuronal endoplasmic reticulum stress potentially via the AMPK/SREBP-1 pathway.Translational research : the journal of laboratory and clinical medicine · 2024Article
- Treadmill training improves lung function and inhibits alveolar cell apoptosis in spinal cord injured rats.Scientific reports · 2024Article
- Crtc1 deficiency protects against sepsis-associated acute lung injury through activating akt signaling pathway.Journal of inflammation (London, England) · 2024Article
- Molecular mechanisms of Sepsis attacking the immune system and solid organs.Frontiers in medicine · 2024Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundBacterial pneumonia and related lung injury are among the most frequent causes of mortality in intensive care units, but also inflict serious and prolonged respiratory complications among survivors. Given that endoplasmic reticulum (ER) stress is a hallmark of sepsis-related alveolar epithelial cell (AEC) dysfunction, we tested if AMP-activated protein kinase (AMPK) affects recovery from ER stress and apoptosis of AECs during post-bacterial infection.
methodsIn a murine model of lung injury by P. aeruginosa non-lethal infection, therapeutic interventions included AMPK activator metformin or GSK-3β inhibitor Tideglusib for 96 h. Recovery from AEC injury was evidenced by accumulation of soluble T-1α (AEC Type 1 marker) in BAL fluids along with fluorescence analysis of ER-stress (CHOP) and apoptosis (TUNEL) in lung sections. AMPK phosphorylation status and mediators of ER stress were determined via Immunoblot analysis from lung homogenates. Macrophage-dependent clearance of apoptotic cells was determined using flow cytometry assay.
resultsP. aeruginosa-induced lung injury resulted in accumulation of neutrophils and cellular debris in the alveolar space along with persistent (96 h) ER-stress and apoptosis of AECs. While lung infection triggered AMPK inactivation (de-phosphorylation of Thr172-AMPK), metformin and Tideglusib promptly restored the AMPK activation status. In post infected mice, AMPK activation reduced indices of lung injury, ER stress and related apoptosis of AECs, as early as 24 h post administration of AMPK activators. In addition, we demonstrate that the extent of apoptotic cell accumulation is also dependent on AMPK-mediated clearance of apoptotic cells by macrophages.
conclusionsOur study provides important insights into AMPK function in the preservation of AEC viability after bacterial infection, in particular due reduction of ER-stress and apoptosis, thereby promoting effective recovery from lung injury after pneumonia.
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