HOBOKEN, N.J.--(BUSINESS WIRE)--John Wiley and Sons Inc. (NYSE:JWA) (NYSE:JWB), in partnership with the Federation of American Societ ies for Experimental Biology (FASEB), is pleased to announce a new peer-reviewed, open access journal, FASEB BioAdvances. Launching in 2018 as part of the Wiley Open Access portfolio, FASEB BioAdvances will be edited by Jasna Markovac, Ph.D., of the University of Michigan and California Inst itute of Technology. Dr. Markovac will serve as the publicat ion’s Founding Editor and will lead the effort for the journal on publishing mult i / transdisciplinary research reports from the international community.

The annual meeting of the federation of american societies for experimental biology

Preface (A Warm Welcome to the New Year 2013: From Immunology, Endocrine & Metabolic Agents in Medicinal Chemistry)

Clinical and demographic characteristics of heart failure with preserved ejection fraction in comparison to hypertension without heart failure, elderly with risk factors, and healthy aging in population dwelling individuals = 65 years of age

DNA deletions and clonal mutations drive premature aging in mitochondrial mutator mice

During life, cardiac muscle is capable of remodeling in response to an increased hemodynamic demand through cardiac hypertrophy. However, in most cases, if the stress stimuli become chronic the initially compensatory hypertrophic response evolves towards a pathological condition and heart failure. In this scenario, a therapeutic approach capable of reducing pathological cardiac hypertrophy could be beneficial. 

Growth differentiation factor 11 (GDF11) is circulating factor able to reduce cardiac hypertrophy in mice. It is a member of TGF-β family, and it shares a high level of homology with myostatin (MSTN) a well-studied protein that regulates skeletal muscle mass and apparently minimal activity on cardiac mass. 

Our data showed different protein levels between cardiac and skeletal muscle tissues revealed a higher abundancy of type I TGF-β receptors (ALK4/5/7) in the heart samples. Moreover, ALK7 receptor knockout induced a significant reduction in SMAD3/4 signaling only after GDF11 treatment. These results showed a differential quantity and use of ALKs receptors, possibly explaining the higher GDF11 sensitivity of cardiomyocytes compared to skeletal myocytes.

Using a model of pressure overload-induced cardiac hypertrophy it was possible to further confirm the anti-hypertrophic activity of GDF11. Interestingly, even if with lower potency, this effect was recapitulated also by MSTN, demonstrating that both peptides have overlapping effects on cardiac tissue. Furthermore, aiming to reduce controversies regarding GDF11 and MSTN serum quantifications, we contributed to develop a novel assay based on mass spectrometry that can discriminate and quantify reliably both proteins. Using this method, it was also possible to identify an age-dependent reduction of both GDF11 and MSTN ligand in mice.

In conclusion, GDF11 and MSTN share a common cardiac anti-hypertrophic activity that was not previously expected. Modulation of GDF11/MSTN signaling pathway can be considered for development of novel therapeutic strategies and new biotherapeutics.

Growth Differentiation Factor 11 and Myostatin: Mechanism and Therapeutic Role in Cardiovascular Diseases

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Growth Differentiation Factor 11 and Myostatin: Mechanism and Therapeutic Role in Cardiovascular Diseases