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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Wang, L. Hao, H. Wang, J. Wang, X. Zhang, S. Du, Y. Lv, T. Zuo, L. Li, Y. Liu, H. |
| Description | Author Affiliation: Wang L ( Department of Pathology, Shanxi Medical University, Taiyuan, Shanxi, PR China.); Hao H ( Department of Physiology, Shanxi Medical University, Taiyuan, Shanxi, PR China.); Wang J ( Department of Orthopaedics, Shanxi Dayi Hospital (Shanxi Academy of Medical Sciences), Taiyuan, Shanxi, PR China.); Wang X ( Department of Physiology, Shanxi Medical University, Taiyuan, Shanxi, PR China.); Zhang S ( Department of Pathology, Shanxi Medical University, Taiyuan, Shanxi, PR China.); Du Y ( Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, PR China.); Lv T ( Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, PR China.); Zuo L ( Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Capital Medical University, Beijing, PR China.); Li Y ( Department of Physiology, Shanxi Medical University, Taiyuan, Shanxi, PR China.); Liu H ( Department of Physiology, Shanxi Medical University, Taiyuan, Shanxi, PR China.) |
| Abstract | Cardiomyocyte death is one major factor in the development of heart dysfunction, thus, understanding its mechanism may help with the prevention and treatment of this disease. Previously, we reported that anti-ß1-adrenergic receptor autoantibodies (ß1-AABs) decreased myocardial autophagy, but the role of these in cardiac function and cardiomyocyte death is unclear. We report that rapamycin, an mTOR inhibitor, restored cardiac function in a passively ß1-AAB-immunized rat model with decreased cardiac function and myocardial autophagic flux. Next, after upregulating or inhibiting autophagy with Beclin-1 overexpression/rapamycin or RNA interference (RNAi)-mediated expression of Beclin-1/3-methyladenine, ß1-AAB-induced autophagy was an initial protective stress response before apoptosis. Then, decreased autophagy contributed to cardiomyocyte death followed by decreases in cardiac function. In conclusion, proper regulation of autophagy may be important for treating patients with ß1-AAB-positive heart dysfunction. |
| File Format | HTM / HTML |
| e-ISSN | 20414889 |
| DOI | 10.1038/cddis.2015.237 |
| Journal | Cell Death and Disease |
| Volume Number | 6 |
| Language | English |
| Publisher | Nature Publishing Group |
| Publisher Date | 2015-08-27 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Research Support, Non-u.s. Gov't Ventricular Dysfunction, Left Rats, Wistar Sirolimus Adrenergic Beta-1 Receptor Antagonists Autophagy Antagonists & Inhibitors Cardiomyopathies Genetics Cell Line Myocytes, Cardiac Tor Serine-threonine Kinases Autoantibodies Signal Transduction Gene Expression Regulation Adenine Administration & Dosage Pharmacology Metabolism Drug Effects Chemically Induced Discipline Cell Biology Receptors, Adrenergic, Beta-1 Pathology Animals Apoptosis Regulatory Proteins Immunization, Passive Ventricular Pressure Analogs & Derivatives Apoptosis |
| Content Type | Text |
| Resource Type | Article |
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