ArticleAmerican journal of translational research2023
FOXO1 regulates NLRP3 inflammasome proteins in LPS-induced cardiotoxicity.
Article in American journal of translational research, 2023. 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, 2 citations in OpenAlex.
- TET2 aggravates podocyte mitotic catastrophe and renal injury in diabetic nephropathy via m5C-dependent downregulation of Wee1 and activation of CDK1-cyclinB1 signaling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- FOXO family and neurodegenerative diseases: Mechanisms of action and therapeutic potential.Redox biology · 2026Review
- Betaine improves hyperoxic lung injury through downregulating pulmonary macrophage pyroptosis in newborn mice.Pediatric research · 2026Article
- Notch2 Directs aTreg Cell Fate Toward Immunoregulation or Inflammatory Pyroptosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
5 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveForkhead box protein O1 (FOXO1) has been shown to regulate multiple proteins in various cardiovascular disease processes. However, the effect of FOXO1 on lipopolysaccharide (LPS)-induced cardiotoxicity remains unknown. The aim of this study was to explore the impact of FOXO1 on LPS-induced cardiotoxicity.
methodsRat-derived H9c2 cells were subjected to LPS, and the manipulation of FOXO1 was achieved through overexpression and knockdown using the adeno-associated virus system and siRNA, respectively. Western blotting and quantitative real-time polymerase chain reaction were utilized to examine the inhibitory effect of FOXO1. Cell viability was examined utilizing Cell Counting Kit-8 assay. The changes of apoptosis were examined utilizing Annexin V-FITC/PI method. The levels of pro-inflammatory cytokines, including interleukin (IL)-1β, IL-18, and tumor necrosis factor-α in the H9c2 cells were measured using ELISA kits. Reactive oxygen species (ROS) generation was quantified using the 2'-7'dichlorofluorescin diacetate assay kit.
resultsIn H9c2 cells treated with LPS, FOXO1 expression was downregulated in a dose-dependent and time-dependent manner. Overexpression of FOXO1 attenuated LPS-induced apoptosis, oxidative stress injury, and cardiomyocyte inflammation, while FOXO1 inhibition aggravated these processes. Additionally, FOXO1 was found to regulate LPS-related myocardial injury by downregulating the expression of NLR family pyrin domain-containing 3 (NLRP3).
conclusionFOXO1 overexpression attenuated apoptosis, ROS generation, and inflammation, whereas FOXO1 inhibition aggravated LPS-induced cardiomyocyte injury via the NLRP3 inflammasome signaling pathway.
Indexed as
Identifiers
37692952PMC10492091W4386592033What OpenQuestion holds
Registered trials
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