Molecular therapy for Myocardial Infarction: Lamin A improves myocardial function after myocardial infarction via up regulation of PNUTS/PPP1R10 (Serine/threonine-protein phosphatase 1 regulatory subunit 10), 23/September/2016, 7.48 am

Regenerating the lost pancreatic β-cells in DM patients: MiR-141-3p increases insulin-secreting cell mass and function via down regulation of its target genes, 23/September/2016, 6.45 am
September 23, 2016
Natural product Life-span extension therapy: Berberine, an alkaloid isolated from the roots and bark of herbs, increases life span by suppressing mTOR pathway through up regulation of its target gene, 24/September/2016, 4.44 pm
September 24, 2016
Show all

A recent study from the Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Frankfurt, Germany shows that “MicroRNA-34a regulates cardiac ageing and function.” This study was published in the 7 March  2013 issue of Nature  by Prof Dimmler, Boon, and others.

On the foundation of this interesting finding, Dr L Boominathan PhD, Director-cum-chief Scientist of GBMD, reports that: Molecular therapy for Myocardial Infarction: Lamin A improves myocardial function after myocardial infarction via  up regulation of PNUTS/PPP1R10 (Serine/threonine-protein phosphatase 1 regulatory subunit 10)

Significance:

satisfaction-guaranted-if-not-refunded

Satisfaction guaranteed if not refunded

Given that: (1)  cardiovascular disease is the leading cause of death worldwide; (2) in India, in 2004, 14.6 lakhs deaths (14% of total deaths) were due to ischemic heart disease; and (3) the global economic cost spent in the treatment of cardiovascular disease in 2011 was little more than 10 billion US dollars, there is an urgent need to find: (i)  a way to induce regeneration of adult cardiomyocytes that were lost in Myocardial patients; (ii) a cheaper alternative to the existing expensive drugs; and (iii) a side-effect-free drug.

This study suggests, for the first time, a small molecule-based cardiac regeneration therapy. Lamin A, by increasing the expression of its target gene, it may increase the expression of PNUTS/PPP1R10. Thereby, it may: (1) inhibit DNA damage responses, (2) inhibit telomere shortening; and (3) promote cardiomyocyte survival/regeneration.

Thus, by treating myocardial patients with Lamin A activators, one may prevent ageing-associated (or, stress-associated) decline in cardiac function. Together, this study suggests that pharmacological formulations encompassing “Lamin A activators” may be used to improve cardiac function after myocardial infarction

Idea Proposed/Formulated byDr L Boominathan Ph.D.

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

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

To citeBoominathan, Molecular therapy for Myocardial Infarction: Lamin A improves myocardial function after myocardial infarction via  up regulation of PNUTS/PPP1R10 (Serine/threonine-protein phosphatase 1 regulatory subunit 10), 23/September/2016, 7.47 am,  Genome-2-Bio-Medicine Discovery center (GBMD), http://genomediscovery.org

Courtesy: When you cite drop us a line at info@genomediscovery.org

# Research cooperation

Amount: $300

Undisclosed information: How Lamin A  increases the expression of PNUTS/PPP1R10

Comments are closed.