Up‐regulation of long non‐coding RNA THRIL in coronary heart disease: Prediction for disease risk, correlation with inflammation, coronary artery stenosis, and major adverse cardiovascular events

Qi, Haijun; Shen, Jie; Zhou, Wenping

doi:10.1002/jcla.23196

Cited by 16 publications

(11 citation statements)

References 21 publications

(31 reference statements)

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“…However, this relation between IL-32 and mortality risk has not been reported previously. That there is an intimate association between inflammation and ischemic heart disease is well-known in the literature ( 16-18 ). There are also an increasing number of reports indicating that increased oxidative stress is seen when the vascular system is diseased ( 19 , 20 ).…”

Section: Discussionmentioning

confidence: 95%

Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32

et al. 2020

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One of the major causes of mortality in the western hemisphere is cardiovascular disease. Therefore, a variety of markers to identify those at risk are required. Interleukin-32 (IL-32) is a cytokine that is associated with inflammation. The aim of the current study was to investigate variations in single nucleotide polymorphisms (SNPs) of IL-32 and plasma expression, and their associations with mortality. A population of 486 elderly community-living persons were evaluated. The participants were followed for 7.1 years and underwent a clinical examination and blood sampling. SNP analyses of IL-32 rs28372698 using allelic discrimination and plasma measurement of IL-32, using ELISA, were performed. During the follow-up period, 140 (28.8%) all-cause and 87 (17.9%) cardiovascular deaths were registered. No significant difference between mortality and plasma concentration of IL-32 was observed. The A/A genotype group exhibited significantly higher all-cause mortality (P=0.036), and an almost two-fold increased risk in a multivariate Cox regression model for all-cause and cardiovascular mortality. A highly significant difference in all-cause and cardiovascular mortality between the A/A and the T/T groups was demonstrated (P=0.015 resp. P=0.014). In the present study, the cytokine IL-32 was demonstrated to have prognostic information, with an increased risk of all-cause and cardiovascular mortality for those with the A/A genotype rs28372698 of IL-32. The A/A genotype could therefore be regarded as a possible biomarker for mortality risk that may be used to offer optimized cardiovascular patient handling in the future. However, the present study sample was small, and the results should be regarded as hypothesis-generating.

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Section: Discussionmentioning

confidence: 95%

Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32

et al. 2020

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“…To determine the expression pattern of lncRNAs (MALAT-1, [40] NEAT-1 [41] and THRIL, [42] ), as well as GAPDH and β-actin (as normalization controls for relative quantification),[ 42 , 43 ] cDNA was synthesized using 350 ng of the total RNA as previously described in detail. [44] …”

Section: Methodsmentioning

confidence: 99%

The expression patterns of MALAT-1, NEAT-1, THRIL, and miR-155-5p in the acute to the post-acute phase of COVID-19 disease

Abbasi-Kolli

Nahand

Kiani

et al. 2022

The Brazilian Journal of Infectious Diseases

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“…This mechanism was further demonstrated by Sheng et al ( 115 ) with the observation that Geniposide alleviated hypoxia-induced injury through downregulation of THRIL in H9c2 cells. In addition, THRIL was increased in CAD patients and proved as a biomarker to evaluate CAD risk ( 116 ).…”

Section: Predicted Lncrnas Based On Available Evidencementioning

confidence: 99%

The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction

Zhang

et al. 2021

Front. Cardiovasc. Med.

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Sepsis is a syndrome with life-threatening organ dysfunction induced by a dysregulated host response to infection. The heart is one of the most commonly involved organs during sepsis, and cardiac dysfunction, which is usually indicative of an extremely poor clinical outcome, is a leading cause of death in septic cases. Despite substantial improvements in the understanding of the mechanisms that contribute to the origin and responses to sepsis, the prognosis of sepsis-induced cardiac dysfunction (SICD) remains poor and its molecular pathophysiological changes are not well-characterized. The recently discovered group of mediators known as long non-coding RNAs (lncRNAs) have presented novel insights and opportunities to explore the mechanisms and development of SICD and may provide new targets for diagnosis and therapeutic strategies. LncRNAs are RNA transcripts of more than 200 nucleotides with limited or no protein-coding potential. Evidence has rapidly accumulated from numerous studies on how lncRNAs function in associated regulatory circuits during SICD. This review outlines the direct evidence of the effect of lncRNAs on SICD based on clinical trials and animal studies. Furthermore, potential functional lncRNAs in SICD that have been identified in sepsis studies are summarized with a proven biological function in research on other cardiovascular diseases.

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Up‐regulation of long non‐coding RNA THRIL in coronary heart disease: Prediction for disease risk, correlation with inflammation, coronary artery stenosis, and major adverse cardiovascular events

Cited by 16 publications

References 21 publications

Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32

Increased mortality in the A/A genotype of the SNP rs28372698 of interleukin 32

The expression patterns of MALAT-1, NEAT-1, THRIL, and miR-155-5p in the acute to the post-acute phase of COVID-19 disease

The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction

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