ArticleThe Journal of general physiology2017
Age-related pacemaker deterioration is due to impaired intracellular and membrane mechanisms: Insights from numerical modeling.
Article in The Journal of general physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- Computational insights on drug effects on intrinsic stochasticity of mouse pacemaker cell activity.Biophysical journal · 2025Article
- Synergy between Membrane Currents Prevents Severe Bradycardia in Mouse Sinoatrial Node Tissue.International journal of molecular sciences · 2023Article
- Role of noncoding RNAs in cardiac ageing.Frontiers in cardiovascular medicine · 2023Review
- Slowing down as we age: aging of the cardiac pacemaker's neural control.GeroScience · 2022Review
- Physiological Roles of the Rapidly Activated Delayed Rectifier KInternational journal of molecular sciences · 2021Article
- Calibration of ionic and cellular cardiac electrophysiology models.Wiley interdisciplinary reviews. Systems biology and medicine · 2020Review
- Cardiac Pacemaker Activity and Aging.Annual review of physiology · 2020Review
- A Heart for Diversity: Simulating Variability in Cardiac Arrhythmia Research.Frontiers in physiology · 2018Review
- Modeling pacemaker deterioration with age.The Journal of general physiology · 2017Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Age-related deterioration of pacemaker function has been documented in mammals, including humans. In aged isolated sinoatrial node tissues and cells, reduction in the spontaneous action potential (AP) firing rate was associated with deterioration of intracellular and membrane mechanisms; however, their relative contribution to age-associated deficient pacemaker function is not known. Interestingly, pharmacological interventions that increase posttranslation modification signaling activities can restore the basal and maximal AP firing rate, but the identities of the protein targets responsible for AP firing rate restoration are not known. Here, we developed a numerical model that simulates the function of a single mouse pacemaker cell. In addition to describing membrane and intracellular mechanisms, the model includes descriptions of autonomic receptor activation pathways and posttranslation modification signaling cascades. The numerical model shows that age-related deterioration of pacemaker function is related to impaired intracellular and membrane mechanisms: HCN
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Registered trials
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