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| Year : 2010 | Volume
: 64
| Issue : 1 | Page : 49 |
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The TWEAK-FN14 axis: Opening new doors
Dilip Gude
Department of Cardiology, AMC, Medwin Hospital, Nampally, Hyderabad, AP, India
| Date of Web Publication | 31-Jan-2012 |
Correspondence Address:
Dilip Gude
Department of Cardiology, AMC, 3rd Floor, Medwin Hospital, Chirag Ali Lane, Nampally, Hyderabad, AP-500 001
India
How to cite this article:
Gude D. The TWEAK-FN14 axis: Opening new doors. Indian J Med Sci 2010;64:49 |
Sir,
TWEAK (TNF-like weak inducer of apoptosis, TNFsf 12 and Apo3L) is a multifunctional cytokine (transmembrane protein) regulating inflammation, angiogenesis, myoblast differentiation and atrophy, tumor apoptosis and cell growth, migration, and survival. [1] Its actions are mainly mediated coupling with the TWEAK receptor, fibroblast growth factor (FGF)-inducible 14 kDa protein (Fn14).
The TWEAK/Fn14 axis has been implicated in vascular remodeling, inflammatory responses, and in governing the atherosclerotic lesion size and the prothrombotic complications associated with atherosclerosis by activation of tissue factor, matrix metallo proteinase-9 and plasminogen activator inhibitor-1 expression in vascular cells. [2] The soluble CD163/TWEAK plasma ratio may be a potential biomarker of atherothrombosis in asymptomatic subjects. Rho-associated protein kinase (ROCK) and nuclear factor-kappa beta (NF-κB) probably mediate the beneficial effects of TWEAK in cardiac remodeling. [3] Measurement of serum sTWEAK concentrations improves the prediction of coronary artery disease, advanced non-ischemic heart failure, and adverse short-term outcome in ST-elevation myocardial infarction.
TWEAK also proved beneficial in cancer, tissue repair following acute injury, chronic autoimmune diseases, renal failure, and acute ischemic stroke.
The TWEAK-Fn14 axis is a novel therapeutic target holding promise against cardiovascular complications, atherosclerosis, and many other disorders.
Acknowledgement: I thank my colleagues and staff of Cardiology Department, Medwin Hospital.
| ¤ References | |  |
| 1. | Chorianopoulos E, Rosenberg M, Zugck C, Wolf J, Katus HA, Frey N. Decreased soluble TWEAK levels predict an adverse prognosis in patients with chronic stable heart failure. Eur J Heart Fail 2009;11:1050-6. 
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| 2. | Muñoz-García B, Madrigal-Matute J, Moreno JA, Martin-Ventura JL, López-Franco O, Sastre C, et al. TWEAK-Fn14 interaction enhances plasminogen activator inhibitor 1 and tissue factor expression in atherosclerotic plaques and in cultured vascular smooth muscle cells. Cardiovasc Res 2011;89:225-33.
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| 3. | Chorianopoulos E, Heger T, Lutz M, Frank D, Bea F, Katus HA, et al. FGF-inducible 14-kDa protein (Fn14) is regulated via the RhoA/ROCK kinase pathway in cardiomyocytes and mediates nuclear factor-kappaB activation by TWEAK. Basic Res Cardiol 2010;105:301-13.
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