The discovery of new mechanisms involved in regeneration of cardiac tissue could open the door to new rejuvenative treatments
Heart disease is bad. Of all the existential risks we face, heart disease in its various forms takes the top spot – felling around 17 million people every year. Accompanying heart attacks result in scarring and poor heart function which can exacerbate underlying issues even further, so improving repair following damage is a clear therapeutic target.
New research has uncovered that in zebrafish a specific microRNA, a small molecule which regulates gene activity, may be able to stimulate growth of new heart cells and the removal of scar tissue. While the heart does a reasonable immediate ‘patch job’ following damage, the resulting scar tissue is a short term fix and prevents effective heart beating.
“The concept of organ regeneration fascinates the public, which tends to view it as science fiction. But the zebrafish heart robustly regenerates missing or damaged tissue in as little as 30 to 60 days. Humans share the same genetic material: the same genetic program resides in each of our cells. Our goal is to understand how zebrafish do this so we can unleash our own repair mechanisms through the reawakening of our dormant genetic codes”
This discovery may well be in zebrafish, but many pathways are remarkably similar in animals and a discovery in one often can lead to discovery in another. Humans display considerable longevity in comparison to zebrafish, and certain genetic pathways may simply be silenced. The ability to repair the heart likely wouldn’t have been an evolutionary priority in the past considering the bulk of any human population would probably have been dead by middle age.
Developing new drugs
The discovery builds on previous work by the same team on a drug called ZF143, which has demonstrated the ability to accelerate heart and limb repair in the laboratory. By analysing this particular microRNA further, new drugs could be developed to copy and facilitate reparative gene expression in humans too. Similar drugs could even help patients with muscular dystrophies too.
Read more at MedicalXpress