ArticleExperimental and therapeutic medicine2021
C1q/TNF-related protein 9 decreases cardiomyocyte hypoxia/reoxygenation-induced inflammation by inhibiting the TLR4/MyD88/NF-κB signaling pathway.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- Progress in research on the role of exosomal miRNAs in the diagnosis and treatment of cardiovascular diseases.Frontiers in genetics · 2022Pooled it
- The Role of Skeletal Muscle Mitochondria in NLRP3 Inflammasome Signaling.Biomolecules · 2026Review
- CTRP family in diseases associated with inflammation and metabolism: molecular mechanisms and clinical implication.Acta pharmacologica Sinica · 2023Review
- Article
- KDM2B overexpression prevents myocardial ischemia-reperfusion injury in rats through regulating inflammatory response via the TLR4/NF-κB p65 axis.Experimental and therapeutic medicine · 2022Article
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9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
C1q/TNF-related protein 9 (CTRP9) acts as an adipokine and has been reported to exert numerous biological functions, such as anti-inflammatory and anti-oxidative stress effects, in ischemic heart disease. In the present study, the role of CTRP9 in neonatal rat cardiomyocytes (NRCMs) following hypoxia/reoxygenation (H/R) and the underlying mechanism was investigated. Adenoviral vectors containing CTRP9 or green fluorescent protein were transfected into NRCMs. A H/R model was constructed 2 days after transfection by 2 h incubation under hypoxia followed by 4 h of reoxygenation. Lactate dehydrogenase (LDH), creatine kinase (CK) and CK-myocardial band (CK-MB) levels were detected by a biochemical analyzer using biochemical kits. In addition, cell viability was detected using trypan blue staining to determine the extent of cell injury. Inflammatory cytokines TNF-α, IL-6 and IL-10 were measured by ELISA. Western blotting and reverse transcription-quantitative PCR were used to evaluate the expression levels of CTRP9, toll-like receptor 4 (TLR4), myeloid differentiation primary response (MyD88) and NF-κB. The DNA binding activity of NF-κB was also detected using an electrophoretic mobility shift assay. The results indicated that transfection with adenoviral vectors containing CTRP9 could markedly enhance CTRP9 expression. CTRP9 overexpression increased cell viability and decreased the release of LDH, CK and CK-MB. In addition, CTRP9 overexpression reduced TNF-α and IL-6 levels whilst increasing IL-10 levels, but decreased the expression of TLR4, MyD88 and NF-κB. Furthermore, the DNA binding activity of NF-κB under H/R was also decreased by CTRP9 overexpression. In conclusion, the results of the present study suggested that CTRP9 could protect cardiomyocytes from H/R injury, which was at least partially due to the inhibition of the TLR4/MyD88/NF-κB signaling pathway to reduce the release of inflammatory cytokines.
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