کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8323941 | 1539901 | 2013 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Molecular mechanisms and signaling pathways of angiotensin II-induced muscle wasting: Potential therapeutic targets for cardiac cachexia
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کلمات کلیدی
AT1RAMPKIGF-1POMCAgRPNPYERKChFACEmTORCRHIRS-1IL-65-aminoimidazole-4-carboxamide ribonucleotideSAAAICARTGF-βPI3KMAPK - MAPKROS - ROSangiotensin II type 1 receptor - آنژیوتانسین II نوع 1 گیرندهAngiotensin-converting enzyme - آنژیوتانسین تبدیل آنزیمAngiotensin II - آنژیوتانسین دوinsulin-like growth factor-1 - انسولین مانند عامل رشد 1interleukin-6 - اینترلوکین ۶trh - بازارESRD یا end stage renal disease - بیماری کلیوی در مرحله نهایی End-stage renal disease - بیماری کلیوی در مرحله پایانیtransforming growth factor-β - تبدیل فاکتور رشد βtumor necrosis factor-α - تومور نکروز عامل αAng II - دومserum amyloid A - سرم آمیلوئید AUbiquitin proteasome system - سیستم پروتئازوم UbiquitinSkeletal muscle - عضله اسکلتیTNF-α - فاکتور نکروز توموری آلفاphosphoinositide 3-kinase - فسفینوزیتید 3-کینازcongestive heart failure - نارسایی احتقانی قلبmammalian target of rapamycin - هدف پستانداران رپامایسینthyrotropin-releasing hormone - هورمون آزاد کننده تیروتروپینcorticotropin-releasing hormone - هورمون آزاد کننده کورتیکوتروپینAgouti-related protein - پروتئین مرتبط با Agoutiproopiomelanocortin - پروپیوملانوکورتینCachexia - کاچکسیAMP-activated kinase - کیناز فعال AMPmitogen-activated kinase - کیناز فعال با mitogenReactive oxygen species - گونههای فعال اکسیژنglucocorticoid receptor - گیرنده گلوکوکورتیکوئیدUPS - یو پی اسNeuropeptide Y - یوروپروتئین Y
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Cachexia is a serious complication of many chronic diseases, such as congestive heart failure (CHF) and chronic kidney disease (CKD). Many factors are involved in the development of cachexia, and there is increasing evidence that angiotensin II (Ang II), the main effector molecule of the renin-angiotensin system (RAS), plays an important role in this process. Patients with advanced CHF or CKD often have increased Ang II levels and cachexia, and angiotensin-converting enzyme (ACE) inhibitor treatment improves weight loss. In rodent models, an increase in systemic Ang II leads to weight loss through increased protein breakdown, reduced protein synthesis in skeletal muscle and decreased appetite. Ang II activates the ubiquitin-proteasome system via generation of reactive oxygen species and via inhibition of the insulin-like growth factor-1 signaling pathway. Furthermore, Ang II inhibits 5ⲠAMP-activated protein kinase (AMPK) activity and disrupts normal energy balance. Ang II also increases cytokines and circulating hormones such as tumor necrosis factor-α, interleukin-6, serum amyloid-A, glucocorticoids and myostatin, which regulate muscle protein synthesis and degradation. Ang II acts on hypothalamic neurons to regulate orexigenic/anorexigenic neuropeptides, such as neuropeptide-Y, orexin and corticotropin-releasing hormone, leading to reduced appetite. Also, Ang II may regulate skeletal muscle regenerative processes. Several clinical studies have indicated that blockade of Ang II signaling via ACE inhibitors or Ang II type 1 receptor blockers prevents weight loss and improves muscle strength. Thus the RAS is a promising target for the treatment of muscle atrophy in patients with CHF and CKD. This article is part of a Directed Issue entitled: Molecular basis of muscle wasting.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: The International Journal of Biochemistry & Cell Biology - Volume 45, Issue 10, October 2013, Pages 2322-2332
Journal: The International Journal of Biochemistry & Cell Biology - Volume 45, Issue 10, October 2013, Pages 2322-2332
نویسندگان
Tadashi Yoshida, A. Michael Tabony, Sarah Galvez, William E. Mitch, Yusuke Higashi, Sergiy Sukhanov, Patrice Delafontaine,