ArticleImmunity, inflammation and disease2023
SIRT6 attenuates LPS-induced inflammation and apoptosis of lung epithelial cells in acute lung injury through ACE2/STAT3/PIM1 signaling.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Advances in sirtuin research in lung diseases (Review).International journal of molecular medicine · 2026Review
- Dexmedetomidine alleviates acute lung injury in humans by modulating the JAK1-STAT3 axis.Experimental and therapeutic medicine · 2026Article
- Cycloastragenol reduces inflammation and apoptosis in acute lung injury by inhibiting the NF-κB p65 and Akt pathways.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Sirt6 deficiency promotes senescence and age-associated intervertebral disc degeneration in mice.Bone research · 2025Article
- Luteolin attenuates inflammation and apoptosis in LPS-induced ALI mice by activating the HGF/c-Met pathway.Frontiers in pharmacology · 2025Article
- SIRT6 loss causes intervertebral disc degeneration in mice by promoting senescence and SASP status.bioRxiv : the preprint server for biology · 2024Article
- X-Box binding protein 1 downregulates SIRT6 to promote injury in pancreatic ductal epithelial cells.Immunity, inflammation and disease · 2024Article
- Metabolic mechanisms orchestrated by Sirtuin family to modulate inflammatory responses.Frontiers in immunology · 2024Review
- SIRT6 attenuates LPS-induced inflammation and apoptosis of lung epithelial cells in acute lung injury through ACE2/STAT3/PIM1 signaling.Immunity, inflammation and disease · 2023Article
- Vitamin K2 (MK-7) attenuates LPS-induced acute lung injury via inhibiting inflammation, apoptosis, and ferroptosis.PloS one · 2023Article
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Abstract
backgroundAcute lung injury (ALI) is a severe and fatal respiratory disease. SIRT6 exerts pivotal activities in the process of lung diseases, but whether SIRT6 impacts ALI has not been covered.
methodsLentivirus recombinant expressing vector SIRT6 gene (Lent-SIRT6) was constructed in mice, and there were control, lipopolysaccharide (LPS), LPS + Vehicle, and LPS + Lent SIRT6 groups. RT-qPCR and western blot detected SIRT6 expression in lung tissues. HE staining observed pathological alternations in lung tissues. Wet-to-dry ratio of the lungs was then measured. The cell count of bronchoalveolar lavage fluid (BALF) was evaluated. Serum inflammation was examined with enzyme-linked immunosorbent assay, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), and western blot were to measure apoptosis. Western blot tested the expression of ACE2/STAT3/PIM1 signaling-associated factors. At the cellular level, LPS was used to induce lung epithelial cells BEAS-2B to establish cell injury models. SIRT6 was overexpressed and ACE2 expression was inhibited by cell transfection, and the mechanism of SIRT6 in LPS-induced lung injury model was further explored by Cell Counting Kit-8 (CCK-8), western blot, quantitative reverse-transcription polymerase chain reaction, TUNEL, and other techniques.
resultsThe results of animal experiments showed that SIRT6 overexpression could reduce LPS-induced lung pathological injury, pulmonary edema, and BALF cell ratio and attenuate LPS-induced inflammatory response and cell apoptosis. In the above process, ACE2, STAT3, p-STAT3, and PIM1 expression were affected. In cell experiments, SIRT6 expression was reduced in LPS-induced BEAS-2B cells. Inhibition of ACE2 expression could reverse the inhibitory effect of SIRT6 overexpression on ACE2/STAT3/PIM1 pathway, and cellular inflammatory response and apoptosis.
conclusionSIRT6 eased LPS-evoked inflammation and apoptosis of lung epithelial cells in ALI through ACE2/STAT3/PIM1 signaling.
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