TNF Receptor 1/2 Predict Heart Failure Risk in Type 2 Diabetes Mellitus Patients

Zhang, Ping; Ma, Aiqun; Li, Jiwu; Shao, Liang

doi:10.1536/ihj.16-236

Cited by 16 publications

(9 citation statements)

References 27 publications

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“…Thus, the level of the soluble receptors indicate the level or degree of activation of the TNF pathway (Diez-Ruiz et al, 1995) and imbalance between the soluble receptors and TNFα may result in different clinical outcomes (Aderka, 1996). Similarly to ours, previous studies have reported an increase in the level of sTNFRll in diabetes patients compared to controls (Plomgaard et al, 2007) and being predictive of the most important complications of diabetes including nephropathies (Sharma et al, 2015; Carlsson et al, 2016) and heart failures (Ping et al, 2017). sICAM-1 represent a circulating form of ICAM-1 (CD54) that bind to lymphocyte function-associated antigen (LFA-1) and was associated with different pathological conditions (Witkowska and Borawska, 2004).…”

Section: Discussionsupporting

confidence: 83%

Metformin Monotherapy Downregulates Diabetes-Associated Inflammatory Status and Impacts on Mortality

et al. 2019

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Aging is the main risk factor for developing diabetes and other age-related diseases. One of the most common features of age-related comorbidities is the presence of low-grade chronic inflammation. This is also the case of metabolic syndrome and diabetes. At the subclinical level, a pro-inflammatory phenotype was shown to be associated with Type-2 diabetes mellitus (T2DM). This low to mid-grade inflammation is also present in elderly individuals and has been termed inflammaging. Whether inflammation is a component of aging or exclusively associated with age-related diseases in not entirely known. We used clinical data and biological readouts in a group of individuals stratified by age, diabetes status and comorbidities to investigate this aspect. While aging is the main predisposing factor for several diseases there is a concomitant increased level of pro-inflammatory cytokines. DM patients show an increased level of sTNFRll, sICAM-1, and TIMP-1 when compared to Healthy, Non-DM and Pre-DM individuals. These inflammatory molecules are also associated with insulin resistance and metabolic syndrome in Non-DM and pre-DM individuals. We also show that metformin monotherapy was associated with significantly lower levels of inflammatory molecules, like TNFα, sTNFRI, and sTNFRII, when compared to other monotherapies. Longitudinal follow up indicates a higher proportion of death occurs in individuals taking other monotherapies compared to metformin monotherapy. Together our finding shows that chronic inflammation is present in healthy elderly individuals and exacerbated with diabetes patients. Likewise, metformin could help target age-related chronic inflammation in general, and reduce the predisposition to comorbidities and mortality.

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Section: Discussionsupporting

confidence: 83%

Metformin Monotherapy Downregulates Diabetes-Associated Inflammatory Status and Impacts on Mortality

et al. 2019

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“…[33][34][35] Jnk signaling pathway is an important branch of the MAPK signaling pathway, and plays an important role in many physiological and pathological processes, such as cell cycle, reproduction, apoptosis, and cell stress. 36,37) Schreck, et al revealed that the activation of the Jnk signaling pathway causes p-c-jun to undergo nuclear translocation and up-regulates COX-2 expression, thereby accelerating the process of inflammation. 38) In our study, we explored the effect of miR-223 and Jnk signaling pathway on H9c2 cells.…”

Section: Discussionmentioning

confidence: 99%

Emodin Attenuates Lipopolysaccharide-Induced Injury via Down-Regulation of miR-223 in H9c2 Cells

Yang¹,

Jiang²,

Zhuge³

2019

Int. Heart J.

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Emodin is a natural product extracted from Rheum palmatum. There are few recent studies on emodin in the treatment of myocarditis. This study aimed to investigate the effect of emodin on lipopolysaccharide (LPS)induced inflammatory injury in cardiomyocytes. H9c2 cells were treated with 10 μM of LPS and different concentrations (0, 1, 5, 10, 15, and 20 μM) of emodin. The expression of miR-223 was changed by transient transfection. Thereafter, cell viability, apoptosis, the expression of CyclinD1 and Jnk-associated proteins, and the release of pro-inflammatory factors were assessed by cell Counting Kit-8, flow cytometry analysis, quantitative real-time polymerase chain reaction Western blot, and enzyme-linked immunosorbent assay respectively. The results showed that 20 μM of emodin significantly decreased H9c2 cells viability. LPS significantly damaged H9c2 cells, as cell viability was reduced, CyclinD1 was down-regulated, apoptosis was induced, the release of interleukin-1β (IL-1β), IL-6, and tumor necrosis factor-alpha were increased, and the phosphorylation of Jnk and c-Jun were promoted. Emodin protected H9c2 cells against LPS-induced inflammatory injury. miR-223 expression was significantly up-regulated by LPS exposure, while emodin lessened this up-regulation. LPS-injured H9c2 cells were attenuated by the overexpression of miR-223; emodin has protective actions on LPS-injured H9c2 cells and targets. Besides, SP600125 (an inhibitor of Jnk) eliminated miR-223-modulated inflammatory injury in H9c2 cells. These data demonstrated that emodin could attenuate LPS-induced inflammatory injury and deactivate Jnk signaling pathway through down-regulation of miR-223. (Int Heart J 2019; 60: 436-443)

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“…Ping et al . 23 reported that TNFR2 is associated with heart failure risk in type 2 diabetes mellitus patients. Ham et al .…”

Section: Discussionmentioning

confidence: 99%

The association between TNFR gene polymorphisms and the risk of Hepatitis B Virus-Related Liver Diseases in Chinese population

Chen

Mao

et al. 2018

Sci Rep

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Tumor necrosis factor receptor superfamily 2 (TNFR2) plays an important role in controlling the progression of antiviral and antitumorr. Evidence suggests that TNFR2 is involved in the pathogenesis of HBV-induced liver injury. We therefore examined whether TNFR2 polymorphisms are associated with the risk of HBV-related liver disease in Chinese population. In this case-control study, 115 chronic hepatitis B (CHB) patients, 86 HBV-related liver cirrhosis patients (LC), 272 HBV-related hepatocellular carcinoma patients (HCC) and 269 healthy controls were recruited. TNFR2 rs1061622 and rs1061624 polymorphisms were examined using a polymerase chain reaction-restriction fragment length polymorphism analysis. Binary logistic regression analyses revealed that the A allele of rs1061624 was positively associated with the risk of CHB (AA vs. GG, P = 0.026; AA vs. GA+GG, P = 0.021), LC (AA vs. GG, P = 0.027; AA+GA vs. GG, P = 0.036), and HCC (GA vs. GG, P = 0.046; GA+AA vs. GG, P = 0.031). Moreover, subgroup analysis indicated that male subjects have increased risk in developing CHB and LC. Nevertheless, no association was found between rs1061622 polymorphism and HBV-related liver diseases in the overall or subgroup analyses. Our retrospective study suggests that the TNFR2 rs1061624 polymorphism is associated with HBV-related CHB, LC, and HCC in Chinese population, particularly in males.

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TNF Receptor 1/2 Predict Heart Failure Risk in Type 2 Diabetes Mellitus Patients

Cited by 16 publications

References 27 publications

Metformin Monotherapy Downregulates Diabetes-Associated Inflammatory Status and Impacts on Mortality

Metformin Monotherapy Downregulates Diabetes-Associated Inflammatory Status and Impacts on Mortality

Emodin Attenuates Lipopolysaccharide-Induced Injury via Down-Regulation of miR-223 in H9c2 Cells

The association between TNFR gene polymorphisms and the risk of Hepatitis B Virus-Related Liver Diseases in Chinese population

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