TITLE

Cardiovascular disease: Rejuvenating the ageing heart

AUTHOR(S)
Flemming, Alexandra
PUB. DATE
July 2013
SOURCE
Nature Reviews Drug Discovery;Jul2013, Vol. 12 Issue 7, p503
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
The article discusses research being done on the potential role of growth differentiation factor (GDF) in reversing age-related cardiac hypertrophy. It references a study by F. S. Loffredo et al published in a 2013 issue of "Cell." In this study, a heterochronic parabiosis technique was used to integrate the circulation of old and young mice. Results of the study showed that GDF11 has antihypertrophic properties.
ACCESSION #
88783754

 

Related Articles

  • TAK1 is activated in the myocardium after pressure overload and is sufficient to provoke heart failure in transgenic mice. Zhang, Dou; Gaussin, Vinciane; Taffet, George E.; Belaguli, Narasimhaswamy S.; Yamada, Miho; Schwartz, Robert J.; Michael, Lloyd H.; Overbeek, Paul A.; Schneider, Michael D. // Nature Medicine;May2000, Vol. 6 Issue 5, p556 

    The transforming-growth-factor-β-activated kinase TAK1 is a member of the mitogen-activated protein kinase kinase kinase family, which couples extracellular stimuli to gene transcription. The in vivo function of TAK1 is not understood. Here, we investigated the potential involvement of TAK1...

  • Pumping young blood rejuvenates the hearts of old mice.  // New Scientist;5/18/2013, Vol. 218 Issue 2917, p15 

    The article reports on a study by researcher Amy Wagers and team on the effects of the blood protein GDF11 from young mice on older mice with cardiac hypertrophy, finding that the protein showed therapeutic potential in reversing hypertrophy and reducing the size of the heart.

  • TGF-β1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II. Schultz, Jo El J.; Witt, Sandra A.; Glascock, Betty J.; Nieman, Michelle L.; Reiser, Peter J.; NIx, Stacey L.; Kimball, Thomas R.; Doetschman, Thomas // Journal of Clinical Investigation;3/15/2002, Vol. 109 Issue 6, p787 

    Presents a study which investigated the causal relationship between the levels of tumor growth factor (TGF)-Β1 and cardiac hypertrophy. Role of potent hypertrophic stimulus angiotensin II in TGFβ1 gene expression; Physiologic mechanisms of TGF; Results of echocardiography tests.

  • Pioglitazone Attenuates Cardiac Fibrosis and Hypertrophy in a Rat Model of Diabetic Nephropathy. Elrashidy, Rania A.; Asker, Mervat E.; Mohamed, Hoda E. // Journal of Cardiovascular Pharmacology & Therapeutics;Sep2012, Vol. 17 Issue 3, p324 

    Pioglitazone has been demonstrated to have beneficial effects on cardiovascular outcomes. However, little is known about its effect on cardiac remodeling associated with diabetic nephropathy. Therefore, this study was designed to study the effects of pioglitazone on cardiac fibrosis and...

  • The microRNA-15 family inhibits the TGFβ-pathway in the heart. Tijsen, Anke J.; van der Made, Ingeborg; van den Hoogenhof, Maarten M.; Wijnen, Wino J.; van Deel, Elza D.; de Groot, Nina E.; Alekseev, Sergey; Fluiter, Kees; Schroen, Blanche; Goumans, Marie-José; van der Velden, Jolanda; Duncker, Dirk J.; Pinto, Yigal M.; Creemers, Esther E. // Cardiovascular Research;Oct2014, Vol. 104 Issue 1, p61 

    Aims The overloaded heart remodels by cardiomyocyte hypertrophy and interstitial fibrosis, which contributes to the development of heart failure. Signalling via the TGFβ-pathway is crucial for this remodelling. Here we tested the hypothesis that microRNAs in the overloaded heart regulate this...

  • Shensongyangxin protects against pressure overload-induced cardiac hypertrophy. DI-FEI SHEN; QING-QING WU; JIAN NI; WEI DENG; CONG WEI; ZHEN-HUA JIA; HENG ZHOU; MENG-QIAO ZHOU; ZHOU-YAN BIAN; QI-ZHU TANG // Molecular Medicine Reports;2016, Vol. 13 Issue 1, p980 

    Shensongyangxin (SSYX) is a medicinal herb, which has long been used in traditional Chinese medicine. Various pharmacological activities of SSYX have been identified. However, the role of SSYX in cardiac hypertrophy remains to be fully elucidated. In present study, aortic banding (AB) was...

  • Epigenetic control of signaling networks involved in interleukin-18-induced cardiac hypertrophy and its attenuation by pan-histone deacetylase inhibitors.  // BMC Bioinformatics;2010 Supplement 4, Vol. 11, p1 

    The article reports on a study that examines the epigenetic control of signaling networks in interleukin-18-induced cardiac hypertrophy and its attenuation by pan-histone deacetylase inhibitors (HDACIs) in mice. It highlights the accompaniment of preprogrammed cardiac hypertrophy-specific gene...

  • Cardiac-specific mindin overexpression attenuates cardiac hypertrophy via blocking AKT/GSK3β and TGF-β1–Smad signalling. Yan, Ling; Wei, Xiang; Tang, Qi-Zhu; Feng, Jinghua; Zhang, Yan; Liu, Chen; Bian, Zhou-Yan; Zhang, Lian-Feng; Chen, Manyin; Bai, Xue; Wang, Ai-Bing; Fassett, John; Chen, Yingjie; He, You-Wen; Yang, Qinglin; Liu, Peter P.; Li, Hongliang // Cardiovascular Research;Oct2011, Vol. 92 Issue 1, p85 

    Aims Mindin is a secreted extracellular matrix protein, an integrin ligand, and an angiogenesis inhibitor, other examples of which are all key players in the progression of cardiac hypertrophy. However, its function during cardiac hypertrophy remains unclear. This study was aimed to identify the...

  • Plasma Levels of Transforming Growth Factor-²1 Reflect Left Ventricular Remodeling in Aortic Stenosis. Villar, Ana V.; Cobo, Manuel; Llano, Miguel; Montalvo, Cecilia; González-Vílchez, Francisco; Martín-Durén, Rafael; Hurlé, María A.; Nistal, J. Francisco // PLoS ONE;2009, Vol. 4 Issue 12, p1 

    Background: TGF-β1 is involved in cardiac remodeling through an auto/paracrine mechanism. The contribution of TGF-β1 from plasmatic source to pressure overload myocardial remodeling has not been analyzed. We investigated, in patients with valvular aortic stenosis (AS), and in mice...

Share

Read the Article

Courtesy of THE LIBRARY OF VIRGINIA

Sorry, but this item is not currently available from your library.

Try another library?
Sign out of this library

Other Topics