Key result
Aging is linked to reduced fast sodium current amplitude without cardiomyocyte hypertrophy in killifish.
Why the study?
Aging is associated with cardiac remodeling and increased arrhythmia risk, but age-related changes in cardiomyocyte fast sodium current in fish myocardium are unclear.
In a short-lived fish model, aging is associated with a decrease in the fast sodium current in ventricular cardiomyocytes without structural hypertrophy, which may contribute to an increased risk of age-related arrhythmias.
May link aging to arrhythmia risk via lower sodium channel density; hypothesis-generating for mammalian studies.
Aging is associated with physiological remodeling of the organism, including cardiac tissue, and an increased risk of arrhythmias. We analyzed age-related changes in cardiomyocyte morphology and the fast sodium current (*I* Na), which determines cardiac excitability and conduction velocity, in the ventricular myocardium of the short-lived fish *Nothobranchius furzeri*. Isolated cardiomyocytes from young (2‑month-old) and aged (4‑month-old) fish were examined using light and fluorescence microscopy and the whole-cell patch-clamp technique. Microscopic analysis revealed no evidence of cell hypertrophy or structural changes in the contractile apparatus in cardiomyocytes from aged fish. However, aging was accompanied by a significant decrease in the amplitude of the fast sodium current *I* Na. The absence of changes in the kinetic parameters of the current may be due to a lower density of sodium channels in the cell membrane during aging.
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Filatova et al. (2026) studied Aging. Aging (4-month-old) vs. Young (2-month-old) fish was evaluated on Amplitude of the fast sodium current (INa) and cardiomyocyte morphology. Aging in Nothobranchius furzeri was associated with a significant decrease in the amplitude of the fast sodium current, without evidence of cell hypertrophy or structural changes.
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