A soft electronic device repairs damaged hearts in mice
Targeted gene delivery reduced heart scar burden by 78% and sustained functional recovery over 16 weeks in a mouse model of heart attack.
Edited by Boris Djordjevic · AgingResearch.News
In an experiment in mice with myocardial infarction (heart attack), researchers tested a soft, stretchable electrode array placed on the heart to map scar tissue and deliver reprogramming factors. The device applied directional electrical pulses to deliver molecules directly to scarred zones, converting resident fibroblasts (cells that form scar tissue) into cardiomyocytes (heart muscle cells).
By day 14, the newly induced heart muscle cells made up 8.96% of total heart muscle area using microRNA combinations and 9.03% using messenger RNA, with conversion efficiencies over 40%. The reprogramming restored electrical function, as electrical potentials recovered from 6.81 millivolts in controls to 12.10 millivolts. Over 16 weeks, the mice showed sustained functional recovery, and scar burden was reduced by 78%. Safety tests showed no reprogramming outside the target area and no whole-body toxicity.
Why it matters
Heart attack risk rises with age, and adult mammalian hearts cannot naturally replace muscle tissue lost to injury. Finding ways to safely guide the conversion of scar tissue into functional muscle cells addresses a key challenge in repairing age-related cardiac damage.
Caveats
The findings come from an experiment in mice, and the abstract did not report sample sizes. In addition, the results were presented as a conference abstract rather than a full, peer-reviewed journal article.
The paper
Targeting fibrotic regions for in situ cardiac regeneration
Southern University of Science and Technology
ESC Congress 2026 Abstract, Oct 26, 2026
Presented at ESC Congress 2026
