Effects of intermedin1-53 on myocardial fibrosis
نویسندگان
چکیده
منابع مشابه
Effects of intermedin1-53 on myocardial fibrosis.
Intermedin (IMD) is a member of the calcitonin/calcitonin gene-related peptide (CGRP) family and has similar or more potent cardiovascular actions than adrenomedullin (ADM) and any other CGRP. The aim of the present work is to study the effects of IMD1-53 on cardiac fibroblast fibrosis in vivo and in vitro. Myocardial infarction model was prepared by ligating rats' left anterior descending coro...
متن کاملIntermedin1-53 attenuates abdominal aortic aneurysm by inhibiting oxidative stress.
OBJECTIVE Oxidative stress plays a critical role in the development of abdominal aortic aneurysm (AAA). Intermedin (IMD) is a regulator of oxidative stress. Here, we investigated whether IMD reduces AAA by inhibiting oxidative stress. APPROACH AND RESULTS In angiotensin II-induced ApoE-/- mouse and CaCl2-induced C57BL/6J mouse model of AAA, IMD1-53 significantly reduced the incidence of AAA a...
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Background and Objective: the aim was to investigate the effects of 12 weeks of High Intensity Interval Training (HIIT) and curcumin supplementation on expression levels of FSTL1 and Smad7 and also Type I, III and IV collagens in rat model with myocardial infraction (MI). Methodology: 48 male rats were randomized into five groups of Reference, HIIT, Curcumin, Concomitant (HIIT+ Curcumin) and Co...
متن کاملIntermedin1–53 Protects Against Myocardial Fibrosis by Inhibiting Endoplasmic Reticulum Stress and Inflammation Induced by Homocysteine in Apolipoprotein E-Deficient Mice
AIM Endoplasmic reticulum stress (ERS) and inflammation participate in cardiac fibrosis. Importantly, a novel paracrine/autocrine peptide intermedin1-53 (IMD1-53) in the heart inhibits myocardial fibrosis in rats. However, the mechanisms are yet to be fully elucidated. METHODS Myocardial fibrosis in apolipoprotein E-deficient (ApoE -/-) mice and neonatal rat cardiac fibroblasts (CFs) were ind...
متن کاملIntermedin1–53 enhances angiogenesis and attenuates adverse remodeling following myocardial infarction by activating AMP-activated protein kinase
Adverse ventricular remodeling is a maladaptive response to acute loss of myocardium and an important risk factor for heart failure following myocardial infarction (MI). Intermedin (IMD) is a novel member of the calcitonin/calcitonin gene‑related peptide family, which may possess potent cardioprotective properties. The aim of the present study was to determine whether IMD1‑53, a mature bioactiv...
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ژورنال
عنوان ژورنال: Acta Biochimica et Biophysica Sinica
سال: 2012
ISSN: 1672-9145,1745-7270
DOI: 10.1093/abbs/gms093