ArticlePLoS computational biology2019
A mathematical model of calcium dynamics: Obesity and mitochondria-associated ER membranes.
Article in PLoS computational biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 31 citations in OpenAlex.
- Interdependence of cytosolic and mitochondrial calcium dynamics in a hepatocyte cell due to obesity.Journal of biosciences · 2026Article
- Computational Model of Complex Calcium Dynamics: Store Operated CaCell biochemistry and biophysics · 2025Article
- Cross Talking Calcium, IPCell biochemistry and biophysics · 2024Article
- Spatial mapping of hepatic ER and mitochondria architecture reveals zonated remodeling in fasting and obesity.Nature communications · 2024Article
- Numerical simulation of calcium dynamics dependent ATP degradation, IPJournal of biological physics · 2023Article
- Research progress on endoplasmic reticulum homeostasis in kidney diseases.Cell death & disease · 2023Review
- Integrative modeling of the cell.Acta biochimica et biophysica Sinica · 2022Review
- Adaptive immune cells shape obesity-associated type 2 diabetes mellitus and less prominent comorbidities.Nature reviews. Endocrinology · 2022Review
- Lipid droplet - mitochondria coupling: A novel lipid metabolism regulatory hub in diabetic nephropathy.Frontiers in endocrinology · 2022Review
- Systems modeling predicts that mitochondria ER contact sites regulate the postsynaptic energy landscape.NPJ systems biology and applications · 2021Article
- Mitochondria and Calcium Homeostasis: Cisd2 as a Big Player in Cardiac Ageing.International journal of molecular sciences · 2020Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Multiple cellular organelles tightly orchestrate intracellular calcium (Ca2+) dynamics to regulate cellular activities and maintain homeostasis. The interplay between the endoplasmic reticulum (ER), a major store of intracellular Ca2+, and mitochondria, an important source of adenosine triphosphate (ATP), has been the subject of much research, as their dysfunction has been linked with metabolic diseases. Interestingly, throughout the cell's cytosolic domain, these two organelles share common microdomains called mitochondria-associated ER membranes (MAMs), where their membranes are in close apposition. The role of MAMs is critical for intracellular Ca2+ dynamics as they provide hubs for direct Ca2+ exchange between the organelles. A recent experimental study reported correlation between obesity and MAM formation in mouse liver cells, and obesity-related cellular changes that are closely associated with the regulation of Ca2+ dynamics. We constructed a mathematical model to study the effects of MAM Ca2+ dynamics on global Ca2+ activities. Through a series of model simulations, we investigated cellular mechanisms underlying the altered Ca2+ dynamics in the cells under obesity. We predict that, as the dosage of stimulus gradually increases, liver cells from obese mice will reach the state of saturated cytosolic Ca2+ concentration at a lower stimulus concentration, compared to cells from healthy mice.
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