ArticleAnnals of translational medicine2021
Knockdown of phosphoinositide-dependent kinase 1 (PDK1) inhibits fibrosis and inflammation in lipopolysaccharide-induced acute lung injury rat model by attenuating NF-κB/p65 pathway activation.
Article in Annals of translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers, 1 of them a synthesis that pooled it.
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Who cites it
10 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Macrophage mechanobiology: from sensing to disease.Frontiers in immunology · 2026Pooled it
- An integrated network pharmacology and proteomics approach reveals the anti-fibrotic effect of Fushen Granule on peritoneal fibrosis.BMC complementary medicine and therapies · 2026Article
- Investigation of the protective effect of cilostazol on acute lung injury-mediated inflammation and in silico molecular modelling studies of inflammatory signalling pathway: a repurposing study.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- USP7 promotes endothelial activation to aggravate sepsis-induced acute lung injury through PDK1/AKT/NF-κB signaling pathway.Cell death discovery · 2025Article
- Role and targeting of the AGC kinase family in pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2024Review
- Pulmonary Effects of Traumatic Brain Injury in Mice: A Gene Set Enrichment Analysis.International journal of molecular sciences · 2024Article
- Article
- The effects and mechanisms of the anti-COVID-19 traditional Chinese medicine, Dehydroandrographolide from Andrographis paniculata (Burm.f.) Wall, on acute lung injury by the inhibition of NLRP3-mediated pyroptosis.Phytomedicine : international journal of phytotherapy and phytopharmacology · 2023Article
- Sp1 transcription factor represses transcription of phosphatase and tensin homolog to aggravate lung injury in mice with type 2 diabetes mellitus-pulmonary tuberculosis.Bioengineered · 2022Article
- An Herbal Product Alleviates Bleomycin-Induced Pulmonary Fibrosis in Mice via Regulating NF-κB/TNF-α Signaling in Macrophages.Frontiers in pharmacology · 2022Article
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Abstract
backgroundAcute lung injury (ALI) is a common inflammatory disease of the lung. This study aimed to investigate the effect of 3-phosphoinositide-dependent kinase 1 (PDK1) interference on the levels of fibrosis and proinflammatory factors in lipopolysaccharide (LPS)-induced ALI and discuss the relevant mechanism.
methodsAn ALI model was established by intravenous injection of LPS treatment. A total of 24 Sprague-Dawley (SD) rats were randomly divided into 4 groups: sham group; ALI group; ALI + shRNA-NC group; and ALI + PDK1-shRNA group. Lung injury score, minute ventilation, lung volume, and airway resistance were used to evaluate lung function injury. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect PDK1 messenger RNA (mRNA) level. Western blot was performed to detect expression levels of PDK1, transforming growth factor-β (TGF-β), α-smooth muscle actin (α-SMA), toll-like receptor 4 (TLR4), p65, and myeloid differentiation primary response gene 88 (MyD88). The contents of interleukin-6 (IL-6), inducible nitric oxide synthase (iNOS), tumor necrosis factor-α (TNF-α), and monocyte chemoattractant protein-1 (MCP-1) were detected by enzyme-linked immunosorbent assay (ELISA). The pathological changes and fibrosis of lung tissues were estimated by hematoxylin and eosin (H&E) and Masson staining.
resultsThe results revealed that high lung injury score, low minute ventilation, low lung volume, and small airway resistance were present in the ALI group. Likewise, severe histopathological damage and fibrosis were apparent in the ALI group. Otherwise, contents of TNF-α, iNOS, IL-6, MCP-1, and levels of α-SMA, TGF-β, TLR4, phosphorylated (p)-p65, and MyD88 were enhanced in the ALI group. Interestingly, pathological changes and fibrosis were improved significantly in the ALI + PDK1-shRNA group. Besides, knockdown of PDK1 reduced lung injury score and enhanced minute ventilation, lung volume, and airway resistance. Moreover, knockdown of PDK1 decreased the contents of TNF-α, iNOS, IL-6, MCP-1, and levels of TGF-β, α-SMA, TLR4, p-p65, and MyD88.
conclusionsKnockdown of PDK1 protects LPS-induced ALI via attenuating activation of the nuclear factor-κB (NF-κB)/p65 pathway.
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