scholarly journals Biological aging and coronary artery disease

2012 ◽  
Author(s):  
Jen Lou Cheng ◽  
Shih-Ying Lee
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Biological Aging ◽  
Artery Disease

scholarly journals Therapeutic Value of miRNAs in Coronary Artery Disease

2021 ◽  
Vol 2021 ◽  
pp. 1-16
Author(s):  
Md Sayed Ali Sheikh ◽  
A. Alduraywish ◽  
A. Almaeen ◽  
Mubarak Alruwali ◽  
Raed Alruwaili ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Mirna Gene ◽  
Disease Process ◽  
Vital Role ◽  
Biological Aging ◽  
Cardiovascular Development ◽  
Microrna Profile ◽  
Ischemic Coronary Artery Disease ◽  
Artery Disease

Atherosclerotic ischemic coronary artery disease (CAD) is a significant community health challenge and the principal cause of morbidity and mortality in both developed and developing countries for all ethnic groups. The progressive chronic coronary atherosclerosis is the main underlying cause of CAD. Although enormous progress occurred in the last three decades in the management of cardiovascular diseases, the prevalence of CAD continues to increase worldwide, indicating the need for discovery of deeper molecular insights of CAD mechanisms, biomarkers, and innovative therapeutic targets. Recently, several research groups established that microRNAs essentially regulate various cardiovascular development and functions, and a deregulated cardiac enriched microRNA profile plays a vital role in the pathogenesis of CAD and its biological aging. Numerous studies established that over- or downregulation of a single miRNA gene by ago-miRNA or anti-miRNA is enough to modify the CAD disease process, significantly prevent age-dependent cardiac cell death, and markedly improve cardiac function. In the light of more recent experimental and clinical evidences, we briefly reviewed and discussed the involvement of miRNAs in CAD and their possible diagnostic/therapeutic values. Moreover, we also focused on the role of miRNAs in the initiation and progression of the atherosclerosis plaque as the strongest risk factor for CAD.

scholarly journals Evidence of accelerated epigenetic aging in patients diagnosed with coronary artery disease: Results of the LipidCardio study

2020 ◽  
Author(s):  
Verena Laura Banszerus ◽  
Valentin Max Vetter ◽  
Maximilian König ◽  
Ulf Landmesser ◽  
Ilja Demuth
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Coronary Stenosis ◽  
Smoking Status ◽  
Obstructive Coronary Artery Disease ◽  
Biological Aging ◽  
Epigenetic Clock ◽  
Epigenetic Age ◽  
Artery Disease

AbstractDNA methylation (DNAm) age acceleration, defined as the deviation of chronological and epigenetic age determined by an epigenetic clock, has been proposed as a biomarker of biological aging. To address the above hypothesis in the context of cardiovascular disease, we evaluated whether patients (N=827, mean chronological age: 69.82±11.01 years, DNAm age: 71.91±16.11, residual DNAm age acceleration: 0.00±9.65 years), who were diagnosed with obstructive coronary artery disease (CAD) by coronary angiography were aged prematurely, i.e. had an increase in the DNAm age acceleration, in comparison with patients for whom obstructive CAD was ruled out (controls).Stratified analysis yielded a significant acceleration in DNAm age (determined by a seven cytosine-phosphate-guanine epigenetic clock) in patients diagnosed with obstructive CAD, defined by at least one >50% coronary stenosis (N=588, rDNA age acceleration=0.58±9.47, corrected p= 2.05⨯10−3) compared to control subjects (N=145, residual (r)DNAm age acceleration= -3.11±10.51 years). Moreover, rDNAm age acceleration was significantly associated with systolic blood pressure (ß=0.069, 95% CI 0.027 – 0.112, p= 1.44⨯10−3), sex (ß=-2.438, 95% CI -4.591 - -0.285, p= 2.65⨯10−2), estimated glomerular filtration rate (eGFR, ß=0.040, 95% CI 0.011 – 0.069, p= 6.87⨯10−9) and smoking status (ß=-8.538, 95% CI -10.772 - -6.303, p= 2,45⨯10−13).Across studies, assessing CAD and its risk factors in the context of epigenetic age acceleration findings are remarkably inconclusive. While the here employed seven-cytosine-phosphate-guanine epigenetic clock suggests premature biological aging in CAD patients, compared to controls without coronary stenosis, its association with cardiovascular risk factors was limited.

Elevated level of circulatory sTLT1 induces inflammation through SYK/MEK/ERK signalling in coronary artery disease

2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Chronic Inflammation ◽  
Ex Vivo ◽  
Human Subjects ◽  
Critical Role ◽  
Atherosclerotic Cardiovascular Disease ◽  
Tnf Α ◽  
Artery Disease

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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