Blocking a protein eases electrical heart changes in aged mice
In aged mice, suppressing the protein p300 reduced electrical remodeling in heart tissue and lowered the likelihood of triggering an irregular heartbeat.
Limit: The abstract does not report the sample size, sex, or ages of the mice
Edited by Boris Djordjevic · AgingResearch.News
In an experiment in animals and cells, researchers examined atrial tissue and heart muscle cells from aged mice, along with atrium-derived cells in senescence, a state in which cells stop dividing. They used electrical measurements and biochemical tests to analyze how aging changes heart function.
In both the aged mice and cultured cells, levels of the protein p300 and markers of cell aging rose, while calcium channel currents and electrical impulse duration declined. Knocking down p300 or inhibiting it with curcumin lowered tissue aging and improved electrical signaling. In the aged mice, suppressing p300 also reduced the inducibility of atrial fibrillation, an irregular heartbeat. Furthermore, aging increased levels of Ahnak1, a protein that bound to a calcium channel component; inhibiting p300 reversed this interaction in both systems.
Why it matters
Age-related electrical remodeling in the heart contributes to the development of atrial fibrillation, an irregular rhythm common in older individuals. Uncovering how proteins disrupt cardiac electrical signaling helps clarify the pathways that make aging hearts prone to arrhythmias.
Caveats
The findings come from rodents and cells grown in dishes, which may not capture the full complexity of human cardiac tissue. In addition, the abstract does not report the sample size, sex, or ages of the mice.
The paper
p300/Ahnak1 promotes the depression of ICa,L of atrial myocytes induced by aging
Guangdong Academy of Medical Sciences
Biochimica et Biophysica Acta Molecular Basis of Disease, May 20, 2026
