ArticleMolecular therapy : the journal of the American Society of Gene Therapy2025
TAT-PBX1 fusion protein alleviates LPS-induced acute lung injury via AMPK-TFAM signaling activation.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Mitochondrial-endoplasmic reticulum interactions in lung diseases.Cell death & disease · 2026Review
- Mitochondrial Dysfunction as a Driver of Neurodegeneration in Parkinson's and Huntington's Disease: Molecular Insights and Emerging Interventions.Molecular neurobiology · 2026Review
- Review
- PDHA1 Hyperactivation Orchestrates Metabolic Reprogramming Promoting Endothelial Senescence.Research (Washington, D.C.) · 2026Article
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5 authors.
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Abstract
Acute lung injury (ALI) represents a critical clinical challenge characterized by uncontrolled pulmonary inflammation and disrupted tissue homeostasis, often leading to severe respiratory dysfunction. Current pharmacological interventions and vaccines have demonstrated suboptimal clinical outcomes in modulating disease progression, highlighting the urgent need for innovative therapeutic strategies. A key pathophysiological feature of ALI involves dysregulation of redox homeostasis and excessive pulmonary inflammation. Based on the demonstrated capacity of PBX1 to mitigate reactive oxygen species (ROS)-induced cellular damage, we hypothesized its therapeutic potential for ALI management. Overexpression of PBX1 in A549 cells can alleviate the increase in tumor necrosis factor α, interleukin (IL)-1β, and IL-6 levels caused by lipopolysaccharide (LPS). To circumvent the limitations associated with viral transduction while enabling efficient macromolecular delivery, we engineered a novel TAT-PBX1 fusion protein. In vivo, TAT-PBX1 effectively attenuated LPS-induced ROS accumulation and inflammatory cytokines, while preserving mitochondrial morphology. It restored ATP levels and the NAD
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