The effects of melatonin on neurohormonal regulation in cardiac cachexia: A mechanistic review

The effects of melatonin on neurohormonal regulation in cardiac cachexia: A mechanistic review


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دانشگاه علوم پزشکی تبریز
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نویسندگان: حامد جعفری وایقان , سودا صالح قدیمی , وحید ملکی , محمد علی زاده

کلمات کلیدی: Cachexia; Heart failure; Melatonin; Neurohormone

نشریه: 19611 , 10 , 120 , 2019

اطلاعات کلی مقاله
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نویسنده ثبت کننده مقاله حامد جعفری وایقان
مرحله جاری مقاله تایید نهایی
دانشکده/مرکز مربوطه دانشکده تغذیه
کد مقاله 69657
عنوان فارسی مقاله The effects of melatonin on neurohormonal regulation in cardiac cachexia: A mechanistic review
عنوان لاتین مقاله The effects of melatonin on neurohormonal regulation in cardiac cachexia: A mechanistic review
ناشر 5
آیا مقاله از طرح تحقیقاتی و یا منتورشیپ استخراج شده است؟ بلی
عنوان نشریه (خارج از لیست فوق)
نوع مقاله Review Article
نحوه ایندکس شدن مقاله ایندکس شده سطح یک – ISI - Web of Science
آدرس لینک مقاله/ همایش در شبکه اینترنت

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Heart failure (HF) is one of the prominent health concerns and its morbidity is comparable to many malignancies. Cardiac Cachexia (CC), characterized by significant weight loss and muscle wasting, frequently occurs in progressive stage of HF. The pathophysiology of CC is multifactorial including nutritional and gastrointestinal alterations, immunological and neurohormonal activation, and anabolic/catabolic imbalance. Neurohormones are critically involved in the development of both HF and CC. Melatonin is known as an anti-inflammatory and antioxidant hormone. It seems that melatonin possibly regulates the neurohormonal signaling pathway related to muscle wasting in CC, but limited comprehensive data is available on the mechanistic aspects of its activity. In this paper, we reviewed the reports regarding the role of neurohormones in CC occurrence and possible activity of melatonin in modulation of HF and subsequently CC via neurohormonal regulation. In addition, we have discussed proposed mechanisms of action for melatonin considering its possible interactions with neurohormones. In conclusion, melatonin likely regulates the signaling pathways related to muscle wasting in CC by reducing tumor necrosis factor α (TNF-α) levels and activating the gene expression of insulin-like growth factor 1 (IGF-1). Also, this hormone inhibits the proteolytic pathway by inhibiting nuclear factor kappa B (NF-κB), renin–angiotensin system and forkhead box protein O1 (FOXO1) pathways and could increase protein synthesis by activating Akt and mammalian target of rapamycin (mTOR). To elucidate the positive role of melatonin in CC and exact mechanisms related to muscle wasting more cellular and clinical trial studies are needed.

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نویسنده نفر چندم مقاله
حامد جعفری وایقاناول
سودا صالح قدیمیدوم
وحید ملکیسوم
محمد علی زادهپنجم

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7.pdf1398/08/131287237دانلود
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