Circular RNA helps protect against heart aging in mice
Deleting circHIPK3 impaired heart function in mice; increasing it restored a heart-protective protein and suppressed an aging-associated pathway.
Edited by Boris Djordjevic · AgingResearch.News
Mice genetically engineered to lack circHIPK3 in heart muscle cells developed impaired heart function, scarring and aging-related changes in an animal experiment. In mouse hearts, levels of circHIPK3, a circular RNA molecule, fell with age.
The researchers combined artificial intelligence with animal and cell experiments to study nucleolin, a heart-protective protein. Their analysis indicated that nucleolin could undergo phase separation—when molecules gather into liquid-like droplets—and that this capacity declined with aging. In molecular experiments, circHIPK3 bound to the RNA instructions for making nucleolin, making those instructions more stable. This preserved nucleolin’s phase separation and promoted production of ribosomes, the cell’s protein-making machinery. Raising circHIPK3 levels in knockout mice restored nucleolin levels and suppressed an aging-associated pathway.
Why it matters
Heart muscle cell senescence, a state in which cells stop dividing, contributes to cardiac aging. The researchers proposed circHIPK3 as a potential target for age-related heart dysfunction.
Caveats
The findings came from experiments in mice and cells, not studies in people. This conference abstract gave no sample sizes.
The paper
AI-driven prediction and experimental validation of nucleolin phase separation during aging
First Affiliated Hospital of Soochow University; Yunnan Fuwai cardiovascular Hospital
ESC Congress 2026 Abstract, Oct 26, 2026
Presented at ESC Congress 2026

