Atherosclerosis Pathways are Activated in Pericoronary Adipose Tissue of Patients with Coronary Artery Disease

Konwerski, Michał; Gromadka, Agnieszka; Arendarczyk, Adam; Koblowska, Marta; Iwanicka-Nowicka, Roksana; Wilimski, Radosław; Czub, Paweł; Filipiak‬, Krzysztof J.; Hendzel, Piotr; Zielenkiewicz, Piotr; Opolski, Grzegorz; Mazurek, Tomasz

doi:10.2147/jir.s326769

Cited by 12 publications

(3 citation statements)

References 67 publications

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“…Although PCAT was shown to have great clinical significance in the occurrence and development of CAD [ 8 ], there are several important questions that must be explored in this popular field. The Gensini score is a traditional index used to evaluate the severity of CAD [ 9 ]; however, it is unknown whether PCAT assessment can determine the severity of CAD.…”

Section: Introductionmentioning

confidence: 99%

The correlation of pericoronary adipose tissue with coronary artery disease and left ventricular function

You

Wang

et al. 2022

BMC Cardiovasc Disord

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Objective We sought to investigate the correlation of pericoronary adipose tissue with coronary artery disease and left ventricular (LV) function. Methods Participants with clinically suspected coronary artery disease were enrolled. All participants underwent coronary computed tomography angiography (CCTA) and echocardiography followed by invasive coronary angiography (ICA) within 6 months. Pericoronary adipose tissue (PCAT) was extracted to analyze the correlation with the Gensini score and LV function parameters, including IVS, LVPW, LVEDD, LVESD, LVEDV, LVESV, FS, LVEF, LVM, and LVMI. The correlation between PCAT and the Gensini score was assessed using Spearman’s correlation analysis, and that between the PCAT volume or FAI and LV function parameters was determined using partial correlation analysis. Results One hundred and fifty-nine participants (mean age, 64.55 ± 10.64 years; men, 65.4% [104/159]) were included in the final analysis. Risk factors for coronary artery disease, such as hypertension, diabetes, dyslipidemia, and a history of smoking or drinking, had no significant association with PCAT (P > 0.05), and there was also no correlation between PCAT and the Gensini score. However, the LAD-FAI was positively correlated with the IVS (r = 0.203, P = 0.013), LVPW (r = 0.218, P = 0.008), LVEDD (r = 0.317, P < 0.001), LVESD (r = 0.298, P < 0.001), LVEDV (r = 0.317, P < 0.001), LVESV (r = 0.301, P < 0.001), LVM (r = 0.371, P < 0.001), and LVMI (r = 0.304, P < 0.001). Also, the LCX-FAI was positively correlated with the LVEDD (r = 0.199, P = 0.015), LVESD (r = 0.190, P = 0.021), LVEDV (r = 0.203, P = 0.013), LVESV (r = 0.197, P = 0.016), LVM (r = 0.220, P = 0.007), and LVMI (r = 0.172, P = 0.036), and the RCA-FAI was positively correlated with the LVEDD (r = 0.258, P = 0.002), LVESD (r = 0.238, P = 0.004), LVEDV (r = 0.266, P = 0.001), LVESV (r = 0.249, P = 0.002), LVM (r = 0.237, P = 0.004), and LVMI (r = 0.218, P = 0.008), respectively. Finally, the total volume was positively correlated with FS (r = 0.167, P = 0.042). Conclusion The FAI was positively correlated with the LV function but was not associated with the severity of coronary artery disease.

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Section: Introductionmentioning

confidence: 99%

The correlation of pericoronary adipose tissue with coronary artery disease and left ventricular function

You

Wang

et al. 2022

BMC Cardiovasc Disord

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“…Inhibition of miR-451 in HUVECs has been demonstrated to promote tube formation and increase migration and invasion ( 66 ). miR-548 is downregulated in the pericoronary adipose tissue of coronary artery disease patients ( 67 ). miR-548 downregulated HMGB1 in human amniotic epithelial cells ( 68 ) and activation of HMGB1 in bone marrow stem cells stimulates proliferation and angiogenesis ( 69 ).…”

Section: Discussionmentioning

confidence: 99%

Endothelial cell-derived extracellular vesicles impair the angiogenic response of coronary artery endothelial cells

Carter

Mathiesen

Miller

et al. 2022

Front. Cardiovasc. Med.

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Cardiovascular disease (CVD) is the most prominent cause of death of adults in the United States with coronary artery disease being the most common type of CVD. Following a myocardial event, the coronary endothelium plays an important role in the recovery of the ischemic myocardium. Specifically, endothelial cells (EC) must be able to elicit a robust angiogenic response necessary for tissue revascularization and repair. However, local or distant cues may prevent effective revascularization. Extracellular vesicles (EV) are produced by all cells and endothelium is a rich source of EVs that have access to the main circulation thereby potentially impacting local and distant tissue function. Systemic inflammation associated with conditions such as obesity as well as the acute inflammatory response elicited by a cardiac event can significantly increase the EV release by endothelium and alter their miRNA, protein or lipid cargo. Our laboratory has previously shown that EVs released by adipose tissue endothelial cells exposed to chronic inflammation have angiostatic effects on naïve adipose tissue EC in vitro. Whether the observed effect is specific to EVs from adipose tissue endothelium or is a more general feature of the endothelial EVs exposed to pro-inflammatory cues is currently unclear. The objective of this study was to investigate the angiostatic effects of EVs produced by EC from the coronary artery and adipose microvasculature exposed to pro-inflammatory cytokines (PIC) on naïve coronary artery EC. We have found that EVs from both EC sources have angiostatic effects on the coronary endothelium. EVs produced by cells in a pro-inflammatory environment reduced proliferation and barrier function of EC without impacting cellular senescence. Some of these functional effects could be attributed to the miRNA cargo of EVs. Several miRNAs such as miR-451, let-7, or miR-23a impact on multiple pathways responsible for proliferation, cellular permeability and angiogenesis. Collectively, our data suggests that EVs may compete with pro-angiogenic cues in the ischemic myocardium therefore slowing down the repair response. Acute treatments with inhibitors that prevent endogenous EV release immediately after an ischemic event may contribute to better efficacy of therapeutic approaches using functionalized exogenous EVs or other pro-angiogenic approaches.

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“…The mechanism of CAD has been extensively researched. The underlying mechanism for initiation and progression of atherosclerotic plaques involves multifactorial gene expression, and the alteration of inflammatory factors ( 5 , 6 ). Thus, the association between inflammation and CAD status is well established.…”

Section: Introductionmentioning

confidence: 99%

The relationship between soluble lymphocyte activation gene-3 and coronary artery disease

Xiong

Duan

Zhou

et al. 2022

Front. Cardiovasc. Med.

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BackgroundSoluble lymphocyte activation gene 3 (sLAG3) may be used for diagnosis or prognosis in various diseases. However, the relationship between sLAG3 and coronary artery disease (CAD) are still unclear. This study aimed to investigate the levels of sLAG3 in patients with CAD, and its potential clinical association with the disease.MethodsA total of 66 subjects (49 patients with CAD and 17 control subjects without CAD) were enrolled. The sLAG3 level was measured using enzyme-linked immunosorbent assay (ELISA) kits. Clinical variables included demographics, biochemical markers, coronary angiography status, and ejection fraction of the heart (EF) were collected, and Gensini scores were calculated. LAG3 gene data was extracted from three datasets (GSE23561, GSE61144, GSE60993) in Gene Expression Omnibus (GEO) to compare differential expression between CAD and control subjects.ResultsThe sLAG3 level was significantly lower in the CAD vs. the controls (P < 0.05), and negatively associated with CAD [odds ratio (OR): 0.212, 95% confidential interval (CI): 0.060–0.746, P < 0.05]. Furthermore, the area under the curve (AUC) of sLAG3 level was significant (P < 0.05). The sLAG3 level in subjects with body mass index (BMI) ≥ 24 kg/m2 was lower compared to those with BMI < 24 kg/m2 (P < 0.05). The sLAG3 level was also negatively associated with BMI and diabetes mellitus (P < 0.05), though not associated with the Gensini scores or EF (P > 0.05). Lastly, the LAG3 gene expression in peripheral whole blood of patients with CAD were down-regulated compared to healthy controls (P < 0.05).ConclusionThe sLAG3 level was negatively associated with the occurrence but not severity of CAD. Meanwhile, the sLAG3 was negatively associated with BMI and diabetes mellitus, suggesting the reduced sLAG3 might be a novel risk factor for developing CAD.

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Atherosclerosis Pathways are Activated in Pericoronary Adipose Tissue of Patients with Coronary Artery Disease

Cited by 12 publications

References 67 publications

The correlation of pericoronary adipose tissue with coronary artery disease and left ventricular function

The correlation of pericoronary adipose tissue with coronary artery disease and left ventricular function

Endothelial cell-derived extracellular vesicles impair the angiogenic response of coronary artery endothelial cells

The relationship between soluble lymphocyte activation gene-3 and coronary artery disease

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