Lifespan extension therapy: E2F1 decreases aging-related decline in muscle function and enhances the longevity of mammals via down regulation of myostatin, 11/April/2015, 16.36

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A study from the Department of Orthopaedic Surgery, University of Michigan Medical School, USA; and Department of Molecular & Integrative Physiology, University of Michigan Medical School, USA shows that “Haploinsufficiency of myostatin protects against aging-related declines in muscle function and enhances the longevity of mice.” This study was published in the 15 March  2015 issue of the Journal “Aging cell” (the no.1 journal in aging) by Prof. Faulkner JA, Mendias CL, and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Lifespan extension therapy: E2F1 decreases aging-related decline in muscle function and enhances the longevity of mammals via down regulation of myostatin

Significance:   Myostatin is known to function as a key modulator of muscle mass and function. Prof. Faulkner JA and his team had shown recently that deficiency of myostatin protects against aging-related loss in muscle function and extends the maximum lifespan of mice.

This study suggests, for the first time, that E2F1, by decreasing the expression of its target gene Myostatin, it may protect against aging-related loss of muscle function.  And, thereby, extend the maximum lifespan of mice. Together, this study suggests that E2F1 may enhance longevity by suppressing Myostatin. Thus, pharmacological formulations encompassing “E2F1  activators” may be used to enhance longevity.

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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To citeBoominathan,  Lifespan extension therapy: E2F1 decreases aging-related decline in muscle function and enhances the longevity of mammals via down regulation of myostatin, 11/April/2015, 16.36, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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* Research cooperation

Undisclosed information: How E2F1 suppresses the expression of Myostatin

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