ArticleThe Journal of international medical research2021
Fatty acid-binding protein 4 silencing protects against lipopolysaccharide-induced cardiomyocyte hypertrophy and apoptosis by inhibiting the Toll-like receptor 4-nuclear factor-κB pathway.
Article in The Journal of international medical research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 10 citations in OpenAlex.
- The Adipokine Hypothesis of Heart Failure With a Preserved Ejection Fraction: A Novel Framework to Explain Pathogenesis and Guide Treatment.Journal of the American College of Cardiology · 2025Review
- Fatty Acid Binding Protein 4 Could Be a Linking Biomarker Between Periodontitis and Systemic Diseases.Biomedicines · 2025Article
- The Multifunctional Family of Mammalian Fatty Acid-Binding Proteins.Annual review of nutrition · 2023Review
- Genetic advancements in obesity management and CRISPR-Cas9-based gene editing system.Molecular and cellular biochemistry · 2023Review
- Cardiomyocyte-specific deletion of TLR4 attenuates angiotensin II-induced hypertension and cardiac remodeling.Frontiers in cardiovascular medicine · 2023Article
- Toll-like receptors in cardiac hypertrophy.Frontiers in cardiovascular medicine · 2023Review
- Fatty Acid-Binding Proteins: Their Roles in Ischemic Stroke and Potential as Drug Targets.International journal of molecular sciences · 2022Review
- Targeting Fatty Acid-Binding Protein 4 Improves Pathologic Features of Aortic Stenosis.International journal of molecular sciences · 2022Article
- Adipose-Derived Lipid-Binding Proteins: The Good, the Bad and the Metabolic Diseases.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the effects and potential mechanisms of fatty acid-binding protein 4 (FABP4) in a lipopolysaccharide (LPS)-induced
methodsRat cardiomyocyte H9c2 cells were transfected with small interfering RNA (siRNA) against FABP4 (siFABP4), then induced with LPS. The following parameters were measured: cell viability, lactate dehydrogenase release, cardiac hypertrophy and related marker expression, apoptosis, inflammatory cytokine release and expression, and the activation of Toll-like receptor 4 (TLR4) and nuclear factor-κB (NF-κB) pathways.
resultsLPS increased the mRNA and protein expression of FABP4 in H9c2 cells. FABP4 silencing by siFABP4 significantly inhibited LPS-induced cardiac hypertrophy and reduced the mRNA expression of the myocardial hypertrophy markers atrial natriuretic peptide and brain natriuretic peptide. siFABP4 also attenuated LPS-induced increase in TUNEL-positive apoptotic cells, caspase-3 and caspase-9 activities, and the release and expression of proinflammatory cytokines. Mechanistically, we found that FABP4 silencing inhibited the mRNA and protein expression of TLR4 and suppressed the NF-kappa B signaling pathway, as evidenced by reduced nuclear NF-κB p65 and increased cytoplasmic I-κBα expression in LPS-stimulated H9c2 cells.
conclusionFABP4 silencing reduces LPS-induced cardiomyocyte hypertrophy and apoptosis by down-regulating the TLR4/NF-κB axis.
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