TNF-α −308 G/A variant and susceptibility to chronic obstructive pulmonary disease: A systematic review and meta-analysis

Asl, Mohammad Salimi; Ahmadi, Ali; Salimian, Jafar; Shohani, Sepideh; Jamalkandi, Sadegh Azimzadeh; Ghanei, Mostafa

doi:10.1016/j.cyto.2019.154763

Cited by 8 publications

(7 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Further analysis showed that this association was significant only in the COPD group with frequent exacerbations of the disease. Recently, several metaanalyses have been performed that confirm the association of the allele A in various populations [18]. Considering the data obtained data, one can assume that genetically determined increased TNFA gene expression is a marker of adverse COPD development.…”

Section: Discussionmentioning

confidence: 90%

Association of CRP, CD14, Pro-Inflammatory Cytokines and Their Receptors (TNFA, LTA, TNFRSF1A, TNFRSF1B, IL1B, and IL6) Genes with Chronic Obstructive Pulmonary Disease Development

et al. 2020

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 90%

Association of CRP, CD14, Pro-Inflammatory Cytokines and Their Receptors (TNFA, LTA, TNFRSF1A, TNFRSF1B, IL1B, and IL6) Genes with Chronic Obstructive Pulmonary Disease Development

et al. 2020

View full text Add to dashboard Cite

show abstract

“…This result was similar to that of the 1000 Genomes Project (as shown in Table 3 ) and that reported by Zhang et al (8.20% for Asians and 15.70% for Caucasians) [ 27 ]. Moreover, several meta-analysis studies also indicated that the rs1800629 A allele had a significant association with susceptibility to osteoarthritis [ 28 ], dilated cardiomyopathy [ 27 ], and chronic obstructive pulmonary disease [ 29 ] among the Asian population, but not among the Caucasian population. These findings indicated that the dependent distribution of alleles could partially explain the susceptibility differences in the ethnic background.…”

Section: Discussionmentioning

confidence: 99%

Ethnicity-Stratified Analysis of the Association between TNF-α Genetic Polymorphisms and Acute Kidney Injury: A Systematic Review and Meta-Analysis

Chen

Liu

et al. 2020

BioMed Research International

View full text Add to dashboard Cite

Background. Several studies have reported conflicting findings regarding the association between tumor necrosis factor-alpha (TNF-α) genetic polymorphisms and acute kidney injury (AKI). Therefore, we performed this meta-analysis to further investigate whether TNF-α variants are related to AKI susceptibility. Methods. A comprehensive search of observational studies on the association of TNF-α polymorphism with AKI susceptibility was conducted in the PubMed, Cochrane, and Embase databases through February 10, 2020. Pooled odds ratios (ORs) and 95% corresponding confidence intervals (95% CIs) were analyzed to evaluate the strength of the relationship. Results. A total of 8 studies involving 6694 patients (2559 cases and 4135 controls) were included. Pooled analysis showed a trend of increased risk between the TNF-α rs1800629 variant and AKI (A vs. G: OR 95 % CI = 1.33 0.98 ‐ 1.81 ) among the overall population. Ethnicity-stratified analysis indicated that the TNF-α rs1800629 variant was a risk factor for Asians ( OR 95 % CI = 1.93 1.59 ‐ 2.35 ) while it is not for Caucasians ( OR 95 % CI = 1.04 0.91 ‐ 1.20 ). Additionally, we also found that TNF-α rs1799964 polymorphism was observed to have a significant relationship with AKI risk in Asian patients (C vs. T, OR 95 % CI = 1.26 1.11 ‐ 1.43 ). Conclusions. The TNF rs1800629 polymorphism exhibited a trend toward AKI susceptibility with ethnic differences. The relationship was found to be significant among the Asian population, but not among those of Caucasian origin. Additionally, the TNF-α rs1799964 polymorphism was also related to a significantly increased risk of AKI in Asians.

show abstract

“…China of patients with COPD at the end of the period, and TNF-α inhibitors are also considered as potential therapeutic drugs for COPD (16)(17)(18)(19)(20). Furthermore, the TNF-α 308 gene variation is an independent factor to induce COPD, which has a higher association with Asians than other populations (13,21). Given previous studies, it is known that TNF-α factor plays an important role in COPD.…”

Section: Blocking Tumor Necrosis Factor-α Delays Progression Of Chronic Obstructive Pulmonary Disease In Rats Through Inhibiting Mapk Sigmentioning

confidence: 99%

“…It was found that there are more than 500 genes associated with COPD from several genetic studies on COPD, most of which are associated with oxidative stress and inflammatory response pathway, particularly TNF-α ( 13 ). TNF-α is a type of multi-effective inflammatory factor, which plays an important role in the physiological processes of inflammation, cytotoxicity and immune regulation ( 14 ).…”

Section: Introductionmentioning

confidence: 99%

“…It was also found that the overexpression of TNF-α can not only induce emphysema and pulmonary fibrosis, but also decrease the muscle quality and aggravate the physiological symptoms of patients with COPD at the end of the period, and TNF-α inhibitors are also considered as potential therapeutic drugs for COPD ( 16-20 ). Furthermore, the TNF-α 308 gene variation is an independent factor to induce COPD, which has a higher association with Asians than other populations ( 13 , 21 ).…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Blocking tumor necrosis factor-α delays progression of chronic obstructive pulmonary disease in rats through inhibiting MAPK signaling pathway and activating SOCS3/TRAF1

Feng

Meng

2021

Exp Ther Med

View full text Add to dashboard Cite

The present study was conducted in order to study the detailed molecular mechanism of tumor necrosis factor (TNF)-α in chronic obstructive pulmonary disease (COPD). The rats were treated with cigarette smoke (CS) and lipopolysaccharide (LPS) to establish the COPD model. Next, the changes in lung injury in COPD rats with TNF-α knockdown was tested. Meanwhile, the regulation of TNF-α on MAPK pathway and its downstream molecules (SOCS3/TRAF1) was determined by western blotting. On this basis, the activation of MAPK and inhibition of SOCS3/TRAF1 was also examined. Subsequently, the lung function was tested with the plethysmograph, the cells of bronchoalveolar lavage fluid was counted and classified. Furthermore, lung tissue sections were stained with hematoxylin and eosin to verify whether the treatment of MAPK pathway and downstream molecules affected the effect of TNF-α knockdown on COPD. The present study showed that TNF-α knockdown could alleviate the decrease in the function and inflammatory injury of the lungs of rats with COPD. Western blot analysis verified that TNF-α knockdown could inhibit the activation of MAPK pathway and increase the expression of SOCS3/TRAF1. The following experimental results showed that the relief of lung injury caused by TNF-α knockdown could be deteriorated by activating MAPK pathway. It was also found that the symptom of COPD was decreased following transfection with sh-TNF-α but worsened by SOCS3/TRAF1 knockdown. Overall, TNF-α knockdown inhibited the activation of MAPK pathway and increased the expression of SOCS3/TRAF1, thus delaying the process of COPD.

show abstract

TNF-α −308 G/A variant and susceptibility to chronic obstructive pulmonary disease: A systematic review and meta-analysis

Cited by 8 publications

References 33 publications

Association of CRP, CD14, Pro-Inflammatory Cytokines and Their Receptors (TNFA, LTA, TNFRSF1A, TNFRSF1B, IL1B, and IL6) Genes with Chronic Obstructive Pulmonary Disease Development

Association of CRP, CD14, Pro-Inflammatory Cytokines and Their Receptors (TNFA, LTA, TNFRSF1A, TNFRSF1B, IL1B, and IL6) Genes with Chronic Obstructive Pulmonary Disease Development

Ethnicity-Stratified Analysis of the Association between TNF-α Genetic Polymorphisms and Acute Kidney Injury: A Systematic Review and Meta-Analysis

Blocking tumor necrosis factor-α delays progression of chronic obstructive pulmonary disease in rats through inhibiting MAPK signaling pathway and activating SOCS3/TRAF1

Contact Info

Product

Resources

About