Manipulating Maturity

Shortly after birth, the cells of the heart lose their ability to proliferate, becoming fully mature, life-long contractile cells. Indeed, it’s this lack of self-renewal capability that means any damage to the heart later in life (such as a heart attack), is likely to result in permanent scarring. Scientists have recently discovered a key developmental protein called PRDM16 that drives heart muscle cells to adopt and maintain their mature state. By experimentally increasing or decreasing the amount of PRDM16 in heart cells derived from human induced pluripotent stem cells (pictured), researchers found that the number of mature cells (coloured green) increased and decreased accordingly. These findings suggest that a short-lived inhibition of PRDM16 could become a strategy to treat heart damage, enabling heart cells at the injury site to temporarily repopulate, before they once again mature into fully functional integrated muscle.

Written by Ruth Williams

Ruth Williams

Writer

Ruth is a freelance science journalist based in the US. She's a regular correspondent for The Scientist, and her work has appeared in The Lancet, Nature, Scientific American Mind, BBC Focus and elsewhere. Twitter @rooph

Website

• Image from work by Kanae Tani and colleagues
• Center for iPS Cell Research and Application, Kyoto University, Kyoto, Japan
• Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)
• Research published in Stem Cell Reports, August 2026