scholarly journals Association of polymorphisms in the sex hormone genes with the presence and severity of coronary artery disease

2022 ◽  
Vol 50 (1) ◽  
pp. 22-33
Author(s):  
Neslihan Çoban ◽  
◽  
Aybike Sena Özuynuk ◽  
Aycan Fahri Erkan ◽  
Ayşem Kaya ◽  
...  
Author(s):  
Roopali Khanna ◽  
Avinash Bansal ◽  
Sudeep Kumar ◽  
Naveen Garg ◽  
Satyendra Tewari ◽  
...  

Background Incidence of coronary artery disease (CAD) increases significantly in postmenopausal women, which is assumed to be an imbalance between serum androgen and estrogen levels. However, studies assessing serum sex hormones and CAD are few and have shown conflicting results. Objective To compare serum sex hormone levels and traditional risk factors among postmenopausal women with angiographically proven CAD and without CAD. Method The study included consecutive postmenopausal women undergoing coronary angiography in our institute from May 2016 to June 2017. The clinical and coronary angiographic data and traditional risk factors were assessed. Fasting serum levels of estradiol (E2), testosterone (T), sex hormone-binding globulin (SHBG), dehydroepiandrosterone sulfate (DHEA-S), and insulin were measured. Results A total of 121 postmenopausal women were included in the study; 69 were CAD and 52 without CAD. Single-vessel disease was most common (55.1%), followed by double-vessel disease (24.6%) and triple-vessel disease (20.3%). Women with CAD had significantly lower estradiol/testosterone (E2/T) ratio (3.7 ± 2.6 vs. 5.4 ± 4.2, p = 0.008) compared with non-CAD group. SHBG, DHEA-S, and insulin levels were similar in CAD and non-CAD groups. The serum level of estradiol predicted the E2/T ratio (r = 0.316, p < 0.001) and positively associated with DHEA (r = 0.181, p = 0.047). Testosterone was negatively associated with E2/T ratio (r = – 0.682, p < 0.001). There was no significant correlation of estrogen, testosterone, or E2/T ratio to lipid profile (total cholesterol, HDL, LDL) in women with CAD. Conclusion E2/T ratio was significantly lowered in postmenopausal women with CAD. E2/T ratio may be a used a predictor of CAD in postmenopausal women


2018 ◽  
Vol 275 ◽  
pp. e137-e138
Author(s):  
A.S. Ozuynuk ◽  
N. Coban ◽  
A.F. Erkan ◽  
B. EkicI ◽  
E. Vurgun ◽  
...  

2003 ◽  
Vol 4 (2) ◽  
pp. 26
Author(s):  
K. Kajinami ◽  
R. Sato ◽  
N. Takekoshi ◽  
S. Matsui ◽  
S. Kanemitsu ◽  
...  

Oncotarget ◽  
2017 ◽  
Vol 8 (57) ◽  
pp. 97101-97113 ◽  
Author(s):  
Yajie Meng ◽  
Dilare Adi ◽  
Yun Wu ◽  
Yongtao Wang ◽  
Mayila Abudoukelimu ◽  
...  

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.


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