Key result
Tumor necrosis factor-α decreased HERG current by up to 35% at 100 ng/ml and prolonged action potential duration via TNFR1-mediated reactive oxygen species production.
Why the study?
Does TNF-α impair HERG/IKr function and prolong action potential duration in HEK293 cells and canine cardiomyocytes?
Population
Cloned HERG K+ channel in HEK293 cells and native IKr in canine cardiomyocytes from healthy adult mongrel…
Comparison
Tumor necrosis factor-α at concentrations… vs Control cells without TNF-α exposure.
Design
Preclinical
Authors
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May link TNF-α to arrhythmogenesis in HF; hypothesis-generating, requires human validation before clinical relevance.
Does TNF-α impair HERG/IKr function and prolong action potential duration in HEK293 cells and canine cardiomyocytes?
TNF-α impairs HERG/IKr function via TNFR1 activation and reactive oxygen species generation, providing a potential mechanism for action potential prolongation and arrhythmogenesis in congestive heart failure.
Wang et al. (2004) studied Congestive heart failure. Tumor necrosis factor-α (TNF-α) vs. Control cells (without TNF-α) was evaluated on HERG current (IHERG) and rapid delayed-rectifier K+ current (IKr). Tumor necrosis factor-α decreased HERG current by up to 35% at 100 ng/ml and prolonged action potential duration via TNFR1-mediated reactive oxygen species production.
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