ArticleBiophysical journal2008
A mathematical model of airway and pulmonary arteriole smooth muscle.
Article in Biophysical journal, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 70 citations in OpenAlex.
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- A Compartmental Model for Simulating the Gut-Brain Axis in Gastric Function Regulation.bioRxiv : the preprint server for biology · 2025Article
- Deciphering the underlying mechanisms of the pharyngeal pumping motions inProceedings of the National Academy of Sciences of the United States of America · 2024Article
- Intrapulmonary arterial contraction assay reveals region-specific deregulation of vasoreactivity to lung injuries.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- A complete biomechanical model ofProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Modeling and experimental approaches for elucidating multi-scale uterine smooth muscle electro- and mechano-physiology: A review.Frontiers in physiology · 2022Review
- A multiscale sliding filament model of lymphatic muscle pumping.Biomechanics and modeling in mechanobiology · 2021Article
- Reduced biomechanical models for precision-cut lung-slice stretching experiments.Journal of mathematical biology · 2021Article
- A theoretical model of inflammation- and mechanotransduction-driven asthmatic airway remodelling.Biomechanics and modeling in mechanobiology · 2018Article
- Static and dynamic stress heterogeneity in a multiscale model of the asthmatic airway wall.Journal of applied physiology (Bethesda, Md. : 1985) · 2016Article
- Airway and Parenchymal Strains during Bronchoconstriction in the Precision Cut Lung Slice.Frontiers in physiology · 2016Article
- A biomechanical model for fluidization of cells under dynamic strain.Biophysical journal · 2015Article
- Phenotype, endotype and patient-specific computational modelling for optimal treatment design in asthma.Drug discovery today. Disease models · 2015Article
- Nonlinear compliance modulates dynamic bronchoconstriction in a multiscale airway model.Biophysical journal · 2014Article
- Modelling airway smooth muscle passive length adaptation via thick filament length distributions.Journal of theoretical biology · 2013Article
- A Ca2+- and PKC-driven regulatory network in airway smooth muscle.The Journal of general physiology · 2013Article
- Activation of store-operated calcium entry in airway smooth muscle cells: insight from a mathematical model.PloS one · 2013Article
- Quantifying parenchymal tethering in a finite element simulation of a human lung slice under bronchoconstriction.Respiratory physiology & neurobiology · 2012Article
- A multi-scale approach to airway hyperresponsiveness: from molecule to organ.Frontiers in physiology · 2012Article
- The importance of synergy between deep inspirations and fluidization in reversing airway closure.PloS one · 2012Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Airway hyperresponsiveness is a major characteristic of asthma and is believed to result from the excessive contraction of airway smooth muscle cells (SMCs). However, the identification of the mechanisms responsible for airway hyperresponsiveness is hindered by our limited understanding of how calcium (Ca2+), myosin light chain kinase (MLCK), and myosin light chain phosphatase (MLCP) interact to regulate airway SMC contraction. In this work, we present a modified Hai-Murphy cross-bridge model of SMC contraction that incorporates Ca2+ regulation of MLCK and MLCP. A comparative fit of the model simulations to experimental data predicts 1), that airway and arteriole SMC contraction is initiated by fast activation by Ca2+ of MLCK; 2), that airway SMC, but not arteriole SMC, is inhibited by a slower activation by Ca2+ of MLCP; and 3), that the presence of a contractile agonist inhibits MLCP to enhance the Ca2+ sensitivity of airway and arteriole SMCs. The implication of these findings is that murine airway SMCs exploit a Ca2+-dependent mechanism to favor a default state of relaxation. The rate of SMC relaxation is determined principally by the rate of release of the latch-bridge state, which is predicted to be faster in airway than in arteriole. In addition, the model also predicts that oscillations in calcium concentration, commonly observed during agonist-induced smooth muscle contraction, cause a significantly greater contraction than an elevated steady calcium concentration.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.