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Introduction: What they say

A study from the Cardiac Regeneration and Ageing Lab, School of Life Science, Shanghai University, Shanghai 200444, China shows that “miR-29b contributes to multiple types of muscle atrophy.” This research paper was published, in the 25 May 2017 issue of the journal “Nature communications” [One of the best research journals in Biology with an I.F of 11.329 ], by Prof. Xiao J, Li J and others.


What we say:

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Natural product-derived regenerative therapy for muscle atrophy: Chrysin, isolated from Passiflora caerulea and Passiflora incarnata among others, increases the expression of IGF-1, PI3K(p85a) and B-Myb, decreases the expression of tumor suppressors, promotes regeneration of muscle cells, and reverses muscle atrophy via up regulation of its target gene


From significance of the study to Public health relevance:

Given: (1) that Muscular dystrophy/wasting is a degenerative disease; (2) that Muscular dystrophy/wasting also occur due to a number of pathophysiological conditions, including cancer, denervation, disuse and fasting ; (3) that there is no permanent cure for muscular dystrophy; (4)  the life-long discomfort and the medical care required to alleviate pain-associated (muscle weakness) with muscular dystrophy; and (5) the global economic cost spent for muscular dystrophy is enormous, there is an urgent need to find: (i) a way to rejuvenate muscle (satellite) stem cells that were lost in Muscular dystrophy; (ii) a cheaper alternative to the existing expensive drugs; and (iii) a side-effect-free natural product-based drug.


What is known?

Prof. Xiao’s research team members has shown that miRNA-29b:(1) promotes skeletal muscle atrophy; and (2) decreases the expression of IGF-1, PI3K(p85a) and B-Myb. While inhibition of MiR-29b expression: (i) stifles atrophy induced by dexamethasone (Dex), TNF-a and H2O2 treatment; (ii) increases phosphorylations of AKT (Ser-473), FOXO3A (Ser-253), mTOR and P70S6K; (iii) decreases expression of Foxo transcription factors; (iv) inhibits ubiquitin ligase expression; (v) suppresses protein degradation; (vi) increases protein synthesis; (vii) augments the expression of myosin isoforms, including Myh7; (vii) stimulates muscle regeneration, growth, and proliferation, suggesting that inhibition of MiR-29b expression in muscles may attenuate muscular dystrophy.


From Research findings to Therapeutic opportunity:

This study suggests, for the first time, a natural product-based therapy for Muscle dystrophy.

Avicularin, by increasing the expression of its target genes, it may decrease the expression of MiR-29b etc. (Fig. 1). Thereby, it may: (1) increase the expression of IGF-1, PI3K(p85a) and B-Myb; (2) increase phosphorylations of AKT (Ser-473), FOXO3A (Ser-253), mTOR and P70S6K; (3) decrease the expression of Forkhead Box O3 (FOXO3) and its downstream target genes such as MAFBX etc.,; and (4) promote the expression of myosin isoforms, such as Myh7; (vii) augment muscle regeneration, growth, and proliferation. Thus, pharmacological formulations encompassing “Avicularin or its analogues, either alone or in combination with other drugs, may be used to treat muscular dystrophy (fig.1)

Figure 1. Mechanistic insights into how Avicularin, by decreasing the expression of MiR-29b, may promote regeneration of muscle cells and attenuate muscle dystrophy.


Details of the research findings:

Idea Proposed/Formulated (with experimental evidence) by: Dr L Boominathan Ph.D.

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Undisclosed mechanistic information: How does Avicularin decrease the expression of MiR-29b to re promote regeneration of muscle cells and attenuate muscle dystrophy?
Amount: $ 500#

# Research cooperation

For purchase and payment details, you may reach us at info@genomediscovery.org


References:

Web: http://genomediscovery.org or http://newbioideas.com

Terms & Conditions apply http://genomediscovery.org/registration/terms-and-conditions/

Citation: Boominathan, L., Natural product-derived regenerative therapy for muscle atrophy: Avicularin, isolated from Polygonum aviculare and among others, increases the expression of IGF-1, PI3K(p85a) and B-Myb, decreases the expression of tumor suppressors, promotes regeneration of muscle cells, and reverses muscle atrophy via up regulation of its target gene, 31/July/2017, 1.40 am, Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

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