Soluble ST2 in coronary artery disease: Clinical biomarkers and treatment guidance

Zhang, Junyan; Chen, Zhongxiu; Ma, Min; He, Yong

doi:10.3389/fcvm.2022.924461

Cited by 20 publications

(18 citation statements)

References 55 publications

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“…However, some of our patients may have had more severe gastritis than others, or even subtle symptoms. Unfortunately, we do not have this data.sST2 is a biomarker that has been extensively studied in recent years [ 7 – 9 ]. An association between sST2 and mortality has already been demonstrated in several populations [ 25 , 26 ].…”

Section: Discussionmentioning

confidence: 99%

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sST2 Levels Show No Association with Helicobacter pylori Infection in Asymptomatic Patients: Implications for Biomarker Research

et al. 2023

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Introduction Helicobacter pylori ( H. pylori ) is a prevalent stomach bacterium that can cause a range of clinical outcomes, including gastric cancer. In recent years, soluble suppression of tumorigenicity-2 (sST2) has gained attention as a biomarker associated with various diseases, such as gastric cancer. The purpose of this study was to explore the possible connection between H. pylori infection and sST2 levels in patients who do not exhibit symptoms. Methods A total of 694 patients from the Salzburg Colon Cancer Prevention Initiative (Sakkopi) were included in the study. The prevalence of H. pylori infection was determined by histology, and sST2 levels were measured in serum samples. Clinical and laboratory parameters, such as age, sex, BMI, smoking status, hypertension, and metabolic syndrome, were also collected. Results The median sST2 concentration was similar between patients with (9.62; 7.18–13.44 ng/mL; p = 0.66) and without (9.67; 7.08–13.06 ng/mL) H. pylori . Logistic regression analysis did not show any association (OR 1.00; 95%CI 0.97–1.04; p = 0.93) between sST2 levels and H. pylori infection, which remained so (aOR 0.99; 95%CI 0.95–1.03; p = 0.60) after adjustment for age, sex, educational status, and metabolic syndrome. In addition, sensitivity analyses stratified by age, sex, BMI, smoking status, educational status, and the concomitant diagnosis of metabolic syndrome could not show any association between sST2 levels and H. pylori infection. Conclusion The results indicate that sST2 may not serve as a valuable biomarker in the diagnosis and treatment of H. pylori infection. Our findings are of relevance for further research investigating sST2, as we could not find an influence of asymptomatic H. pylori infection on sST2 concentration. What Is Already Known? Soluble suppression of tumorigenicity-2 (sST2) has gained attention as a biomarker associated with various diseases, such as gastric cancer. What Is New in This Study? The median sST2 concentration was similar between patients with (9.62; 7.18–13.44 ng/mL; p = 0.66) and without (9.67; 7.08–13.06 ng/mL) H. pylori . What Are the Future Clinical and Research Implications of the Study Findings? The results indicate that sST2 may not serve as a valuable biomarker in the diagnosis and treatment of H. pylori infection.

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Section: Discussionmentioning

confidence: 99%

“…Soluble suppression of tumorigenicity-2 (sST2) is a biomarker that has been extensively studied in recent years [ 7 – 9 ]. It is a member of the interleukin-1 receptor family [ 10 ] and is secreted in response to various forms of cellular stress, including inflammation, tissue injury, and mechanical strain [ 11 ].…”

Section: Introductionmentioning

confidence: 99%

sST2 Levels Show No Association with Helicobacter pylori Infection in Asymptomatic Patients: Implications for Biomarker Research

et al. 2023

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“…Although a large number of studies have shown that the increase of circulating sST2 is of great signi cance in the diagnosis and prognosis of myocardial infarction, hypertension, diabetes, pulmonary hypertension, myocardial hypertrophy and heart failure, the understanding of IL33/ST2 in the cardiovascular eld is still controversial. In particular, there are completely different views on the pathophysiological role of cardiomyocytes [10][11][12][13][14][15]. RND3, also known as RhoE, is a member of the Rho GTP protein superfamily.…”

Section: Introductionmentioning

confidence: 99%

Mechanistic role of RND3-regulated IL33/ST2 signaling on cardiomyocyte senescence

Zhu

Luo

et al. 2023

Preprint

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BACKGROUND: Hyperinflammatory responses are pivotal in the pathophysiology of cardiomyocyte senescence, with IL33 serving as a crucial pro-inflammatory mediator. Our previous findings highlighted RND3's suppressive effect on IL33 expression. This study delves into the influence of RND3 on IL33/ST2 signaling activation and cardiomyocyte senescence. METHODS: AC16 cardiomyocytes were subjected to treatments involving recombinant IL33, NF-κB inhibitor PDTC, or ST2 antibody Astegolimab. SA-β-gal and γH2AX staining were utilized to monitor alterations in cell senescence and DNA damage, respectively. Western blot analysis was conducted to ascertain the expression of Senescence-Associated Secretory Phenotype (SASP) and NF-κB activation. Utilizing CRISPR/Cas9 technology, the RND3 gene was knocked out in H9C2 cells, followed by senescence analysis and sST2 level detection in the culture medium supernatant via ELISA. Post-AAV9 injection overexpressing RND3 in SD rats, IL33/ST2 and SASP expression in heart tissues, and serum IL33 and sST2 changes were evaluated using ELISA. RESULTS: Exogenous IL-33 significantly induced IL-1α, IL6, and MCP1 expression, increased the p-p65/p65 ratio, and the proportion of SA-β-gal and γH2AX positive cells in AC16 cells. PDTC and Astegolimab application mitigated these effects. RND3 knockout in H9C2 cells led to increased intracellular IL33, ST2L, IL1 α, IL6, and MCP1 expression, decreased sST2 in the supernatant, and increased SA-β-gal and γH2AX positive cells. RND3 overexpression suppressed IL33, ST2L, IL-1α, IL6, and MCP1 expression in heart tissues, decreased serum IL33, and increased sST2 levels. CONCLUSION: RND3 expression in cardiomyocytes modulates cell senescence by negatively regulating the IL33/ST2/NF-κB signaling pathway, underscoring its potential as a therapeutic target in cardiovascular senescence.

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“…Recent studies have shown that recombinant sST2 promotes mitochondrial fusion in human cardiac broblasts, increasing oxidative stress and the secretion of in ammatory cytokines [11]. High levels of sST2 have been found to be associated with poor prognosis of cardiac brosis and cardiomyopathy, which can be used as an independent predictor of heart disease [12][13][14].…”

Section: Introductionmentioning

confidence: 99%

sST2: A bridge between Sirt1/p53/p21 signal-induced senescence and TGF-β1/Smad2/3 regulation of cardiac fibrosis in mice viral myocarditis

Tan

Wei²,

2022

Preprint

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Soluble interleukin 1 receptor-like 1 (sST2) is a novel predictor of poor outcomes, which is involved in inflammatory response and fibrosis of myocarditis. Cardiac fibrosis is a major cause of cardiovascular disease. Cellular senescence is a state of irreversible cell cycle arrest and studies have shown that senescence of myofibroblasts can limit or reduce myocardial fibrosis. Previous studies show that cellular senescence is associated with the progress of myocarditis, and cardiac fibroblasts is closely related to cardiac fibrosis. Therefore, we investigated the role of sST2 on senescence and fibrosis in mice cardiac fibroblasts (MCF). Meanwhile, its pathological role in mice viral myocarditis (VMC) was also investigated. In vitro experiments revealed that sST2 is beneficial to activate MCF by TGF-β1/Smad2/3 signaling and inhibit cell senescence by Sirt1/P53/P21 signaling pathway. CVB3-infected mice exhibited an increased deposition of collagen in the heart and decreased MCF senescence compared to WT mice while these pathological effects are reversed by anti-ST2 mAb. In addition, we found that inhibiting the senescence of MCF is beneficial to cardiac fibrosis and this effect is achieved by paracrine action. The present study reveals a new pathogenic pathway, sST2, which leads to cardiac fibrosis of VMC by inhibiting MCF senescence.

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Soluble ST2 in coronary artery disease: Clinical biomarkers and treatment guidance

Cited by 20 publications

References 55 publications

sST2 Levels Show No Association with Helicobacter pylori Infection in Asymptomatic Patients: Implications for Biomarker Research

sST2 Levels Show No Association with Helicobacter pylori Infection in Asymptomatic Patients: Implications for Biomarker Research

Mechanistic role of RND3-regulated IL33/ST2 signaling on cardiomyocyte senescence

sST2: A bridge between Sirt1/p53/p21 signal-induced senescence and TGF-β1/Smad2/3 regulation of cardiac fibrosis in mice viral myocarditis

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