| Literature DB >> 24184665 |
Telma Martins1, Rui Vitorino2, Daniel Moreira-Gonçalves3, Francisco Amado4, José Alberto Duarte3, Rita Ferreira1.
Abstract
Cardiac cachexia (CC) affects a large proportion of patients with chronic heart failure, a major public health issue in western countries. The pathophysiology of CC is complex and multifactorial, resulting from several factors interacting in a complex system with metabolic, immune and neurohormonal consequences, triggered to protect the heart and the circulation from damage. Despite the adverse clinical effects, CC diagnosis is not straightforward and has not specifically been targeted, with therapeutic strategies only comprising interventions with appetite stimulants, and anti-inflammatory substances. Here we review the molecular pathways underlying CC-related muscle wasting aiming to provide clues for the definition of CC-specific biomarkers and for the development of drugs that prevent and/or counteract muscle impairment, which will certainly impact the management of cardiovascular disorders.Entities:
Keywords: 4E-BP1; ACE; ANP; Angiotensin-converting enzyme; Atrial natriuretic peptide; BMD; BMI; BNP; Body mass index; Bone mineral density; Brain natriuretic peptide; CC; CHF; CT; Cardiac cachexia; Chronic heart failure; Computed tomography; Constitutive nitric oxide synthase; DHEA; Dehydroepiandrosterone; ESR; Erythrocyte sedimentation rate; Eukaryotic translation initiation factor 4E binding protein; FOXO; Forkhead box O; GC; GFR; GH; Glomerular filtration rate; Glucocorticoids; Growth hormone; HF; Heart failure; IGF; IGFBP-3; IGFBPs; IL-1; IL-10; IL-1β; IL-6; Inhibitor of the eukaryotic translation initiation factor 4E; Insulin-like growth factor; Insulin-like growth factor binding protein 3; Insulin-like growth factor binding proteins; Interleukin 1; Interleukin 1 beta; Interleukin 10; Interleukin 6; LPS; MRI; Magnetic resonance imaging; Mechanisms; N-terminal pro-BNP; NOS; NPS; NT-proBNP; Natriuretic peptide system; Nitric oxide synthase; PI3K; PNS; PRA; Parasympathetic nervous system; Phosphatidylinositol 3-kinase; Plasma renin activity; RAAS; ROS; Reactive oxygen species; Renin–angiotensin–aldosterone system; SNS; Soluble form of tumor necrosis factor receptor; Sympathetic nervous system; TGF-β1; TNF-α; TNFRs; Transforming growth factor beta 1; Tumor necrosis factor alpha; Tumor necrosis growth factor receptors; UPP; Ubiquitin–proteasome pathway; cNOS; eIF-4E; lipopolysaccharide; p70 ribosomal protein S6 kinase 1; p70S6K1; sTNFR
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Year: 2013 PMID： 24184665 DOI： 10.1016/j.clinbiochem.2013.10.025
Source DB: PubMed Journal: Clin Biochem ISSN： 0009-9120 Impact factor: 3.281