scholarly journals The Tumor Necrosis Factor Superfamily of Cytokines in the Inflammatory Myopathies: Potential Targets for Therapy

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
Boel De Paepe ◽  
Kim K. Creus ◽  
Jan L. De Bleecker
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Current Knowledge ◽  
Inflammatory Diseases ◽  
Inflammatory Myopathies ◽  
Necrosis Factor Alpha ◽  
Tnf Superfamily ◽  
Sporadic Inclusion Body Myositis ◽  
Factor Alpha ◽  
Necrosis Factor

The idiopathic inflammatory myopathies (IM) represent a heterogeneous group of autoimmune diseases, of which dermatomyositis (DM), polymyositis (PM), and sporadic inclusion body myositis (IBM) are the most common. The crucial role played by tumor necrosis factor alpha (TNFα) in the IM has long been recognized. However, so far, 18 other members of the TNF superfamily have been characterized, and many of these have not yet received the attention they deserve. In this paper, we summarize current findings for all TNF cytokines in IM, pinpointing what we know already and where current knowledge fails. For each TNF family member, possibilities for treating inflammatory diseases in general and the IM in particular are explored.

scholarly journals The Role of TNF-αand TNF Superfamily Members in the Pathogenesis of Calcific Aortic Valvular Disease

2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Antonella Galeone ◽  
Domenico Paparella ◽  
Silvia Colucci ◽  
Maria Grano ◽  
Giacomina Brunetti
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Experimental Studies ◽  
Calcific Aortic Valve Disease ◽  
Necrosis Factor Alpha ◽  
Major Morbidity ◽  
Tnf Superfamily ◽  
Factor Alpha ◽  
Necrosis Factor

Calcific aortic valve disease (CAVD) represents a slowly progressive pathologic process associated with major morbidity and mortality. The process is characterized by multiple steps: inflammation, fibrosis, and calcification. Numerous studies focalized on its physiopathology highlighting different “actors” for the multiple “acts.” This paper focuses on the role of the tumor necrosis factor superfamily (TNFSF) members in the pathogenesis of CAVD. In particular, we discuss the clinical and experimental studies providing evidence of the involvement of tumor necrosis factor-alpha (TNF-α), receptor activator of nuclear factor-kappa B (NF-κB) ligand (RANKL), its membrane receptor RANK and its decoy receptor osteoprotegerin (OPG), and TNF-related apoptosis-inducing ligand (TRAIL) in valvular calcification.

scholarly journals The characterization of tumor necrosis factor alpha (TNF-α), its role in cancerogenesis and cardiovascular system diseases and possibilities of using this cytokine as a molecular marker

2017 ◽  
Vol 13 ◽  
pp. 1-8 ◽  
Author(s):  
Beniamin Grabarek ◽  
Martyna Bednarczyk ◽  
Urszula Mazurek
Keyword(s):  
Tumor Necrosis Factor ◽  
Molecular Marker ◽  
Tumor Necrosis Factor Alpha ◽  
Tumor Necrosis ◽  
Inflammatory Diseases ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
The Impact ◽  
Necrosis Factor

The inflammatory process is directly associated with secretion of cytokines, e.g. tumor necrosis factor alpha (TNF-α). This molecule is one of the 22 proteins which belong to TNF family and is secreted mainly by: macrophages, monocytes, T lymphocyte and mast cells. The biological effects of TNF-α is possible through binding this cytokine to specific receptors – TNFR1 and TNFR2. The large number of reports provides that this cytokine plays extremely important role in cancers and cardiovascular disease – two groups of inflammatory diseases. Unfortunately, these diseases are the main cause of death in spite of advances in medicine and increasing public awareness of prevention. It is believed that better understanding both molecular potential of this cytokine and the impact in cancerogenesis and others inflammatory diseases may cause using TNF-α as a molecular marker in these diseases and will make it possible to observe the effects of anti-inflammatory therapy. It will be able to cause a drop in the incidence of these diseases and better monitoring of them.

scholarly journals Tumor Necrosis Factor Alpha: A Link between Neuroinflammation and Excitotoxicity

2014 ◽  
Vol 2014 ◽  
pp. 1-12 ◽  
Author(s):  
Gabriel Olmos ◽  
Jerònia Lladó
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis Factor Alpha ◽  
Ampa Receptors ◽  
Tumor Necrosis ◽  
Molecular Mechanisms ◽  
De Novo ◽  
Current Knowledge ◽  
Necrosis Factor Alpha ◽  
Factor Alpha ◽  
Necrosis Factor

Tumor necrosis factor alpha (TNF-α) is a proinflammatory cytokine that exerts both homeostatic and pathophysiological roles in the central nervous system. In pathological conditions, microglia release large amounts of TNF-α; thisde novoproduction of TNF-αis an important component of the so-called neuroinflammatory response that is associated with several neurological disorders. In addition, TNF-αcan potentiate glutamate-mediated cytotoxicity by two complementary mechanisms: indirectly, by inhibiting glutamate transport on astrocytes, and directly, by rapidly triggering the surface expression of Ca+2permeable-AMPA receptors and NMDA receptors, while decreasing inhibitory GABAAreceptors on neurons. Thus, the net effect of TNF-αis to alter the balance of excitation and inhibition resulting in a higher synaptic excitatory/inhibitory ratio. This review summarizes the current knowledge of the cellular and molecular mechanisms by which TNF-αlinks the neuroinflammatory and excitotoxic processes that occur in several neurodegenerative diseases, but with a special emphasis on amyotrophic lateral sclerosis (ALS). As microglial activation and upregulation of TNF-αexpression is a common feature of several CNS diseases, as well as chronic opioid exposure and neuropathic pain, modulating TNF-αsignaling may represent a valuable target for intervention.

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