The Emerging Role of MicroRNA-155 in Cardiovascular Diseases
نویسندگان
چکیده
MicroRNAs have been demonstrated to be involved in human diseases, including cardiovascular diseases. Growing evidences suggest that microRNA-155, a typical multifunctional microRNA, plays a crucial role in hematopoietic lineage differentiation, immunity, inflammation, viral infections, and vascular remodeling, which is linked to cardiovascular diseases such as coronary artery disease, abdominal aortic aneurysm, heart failure, and diabetic heart disease. The effects of microRNA-155 in different cell types through different target genes result in different mechanisms in diseases. MicroRNA-155 has been intensively studied in atherosclerosis and coronary artery disease. Contradictory results of microRNA-155 either promoting or preventing the pathophysiological process of atherosclerosis illustrate the complexity of this pleiotropic molecule. Therefore, more comprehensive studies of the underlying mechanisms of microRNA-155 involvement in cardiovascular diseases are required. Furthermore, a recent clinical trial of Miravirsen targeting microRNA-122 sheds light on exploiting microRNA-155 as a novel target to develop effective therapeutic strategies for cardiovascular diseases in the near future.
منابع مشابه
سلولهای بنیادی قلبی در یک نگاه: مقاله مروری
It was assumed that the loss of cardiomyocytes is irreversible. The main goal is to develop widely available and clinically applicable treatments for heart diseases. The several studies have showed that the use of stem cells can improve complicacies such as cardiovascular diseases. Stem cells have a potential benefit of the self-renewal and cell differentiation into the cell types that can play...
متن کاملThe role of microRNA in acute/chronic, myeloid/lymphocytic leukemia
MicroRNAs are small, non-coding sequences that regulate gene expression by inducing degradation or translational inhibition of target mRNAs. These molecules control many intracellular physiological and pathological processes.Abnormal expression of these moleculs has been described in different cancers including hematopoietic cancers. According to the type of cancer and the stage, miRNA’s expres...
متن کاملSilencing MicroRNA-155 Attenuates Cardiac Injury and Dysfunction in Viral Myocarditis via Promotion of M2 Phenotype Polarization of Macrophages
Macrophage infiltration is a hallmark feature of viral myocarditis. As studies have shown that microRNA-155 regulates the differentiation of macrophages, we aimed to investigate the role of microRNA-155 in VM. We report that silencing microRNA-155 protects mice from coxsackievirus B3 induced myocarditis. We found that microRNA-155 expression was upregulated and localized primarily in heart-infi...
متن کاملInhibition of microRNA-155 ameliorates cardiac fibrosis in the process of angiotensin II-induced cardiac remodeling
Cardiac fibrosis triggered by pressure overload represents one of the major challenges in the treatment of cardiovascular diseases. MicroRNA (miRNA/miR)‑155, a member of the small RNA family, has previously been demonstrated to be associated with cardiac inflammation. However, the effect of miR‑155 on cardiac fibrosis induced by angiotensin II (Ang II), particularly in cardiac fibroblasts, requ...
متن کاملmiR-155 acts as an anti-inflammatory factor in atherosclerosis-associated foam cell formation by repressing calcium-regulated heat stable protein 1.
Atherosclerosis (AS) is chronic inflammation in response to lipid accumulation. MicroRNA-155 (miR-155) is being increasingly studied to evaluate its potential as diagnostic biomarkers and therapeutic targets in many diseases. However, delineating the role of miR-155 in AS remains difficult. Here, we detected constitutive expression of several microRNAs (miRNAs) possibly associated with cardiova...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
دوره 2016 شماره
صفحات -
تاریخ انتشار 2016