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模拟淋巴管平滑肌细胞中的起搏器振荡:两种不同系统效应导致动作电位延长。

Modelling pacemaker oscillations in lymphatic muscle cells: lengthened action potentials by two distinct system effects.

作者信息

Hancock Edward J, Macaskill Charlie, Zawieja Scott D, Davis Michael J, Bertram Christopher D

机构信息

School of Mathematics & Statistics, University of Sydney, Sydney, New South Wales 2006, Australia.

Department of Medical Pharmacology & Physiology, University of Missouri, Columbia, MO 65212, USA.

出版信息

R Soc Open Sci. 2025 Jan 8;12(1):241714. doi: 10.1098/rsos.241714. eCollection 2025 Jan.

Abstract

Lymphatic system failures contribute to cardiovascular and various other diseases. A critical function of the lymphatic vascular system is the active pumping of fluid from the interstitium back into the blood circulation by periodic contractions of lymphatic muscle cells (LMCs) in the vessel walls. As in cardiac pacemaking, these periodic contractions can be interpreted as occurring due to linked pacemaker oscillations in the LMC membrane potential (M-clock) and calcium concentration (C-clock). We previously reported a minimal model of synchronized dual-clock-driven oscillations. While this qualitatively replicated the period of oscillations under different conditions, it did not replicate the action potential shape as it varied under those conditions, particularly as regards the extent or lack of a systolic plateau. Here, we modify the model to replicate the plateau behaviour. Using phase-plane analysis we show two qualitatively different dynamical mechanisms that could account for plateau formation, one largely M-clock-driven, the other largely C-clock-driven. The second case occurs with the introduction of a ryanodine receptor; in both cases, we find improved predictions for calcium levels. With enhanced fidelity to the experimental data, the improved model has the potential to help determine opportunities for pharmacological treatment of lymphatic system pumping defects.

摘要

淋巴系统功能障碍会导致心血管疾病和其他多种疾病。淋巴管系统的一项关键功能是通过血管壁中淋巴肌细胞(LMCs)的周期性收缩,将间质中的液体主动泵回血液循环。与心脏起搏类似,这些周期性收缩可被解释为是由于LMC膜电位(M时钟)和钙浓度(C时钟)中相互关联的起搏器振荡所致。我们之前报道过一个同步双时钟驱动振荡的最小模型。虽然该模型定性地复制了不同条件下的振荡周期,但并未复制出在这些条件下变化的动作电位形状,尤其是在收缩期平台的程度或有无方面。在此,我们对模型进行修改以复制平台行为。通过相平面分析,我们展示了两种性质不同的动力学机制,它们可以解释平台的形成,一种主要由M时钟驱动,另一种主要由C时钟驱动。第二种情况是在引入ryanodine受体时出现的;在这两种情况下,我们发现对钙水平的预测有所改善。随着对实验数据保真度的提高,改进后的模型有潜力帮助确定治疗淋巴系统泵血缺陷的药物治疗机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8438/11706657/a95089102d48/rsos.241714.f001.jpg

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