期刊
BIOPHYSICAL JOURNAL
卷 96, 期 4, 页码 1318-1332出版社
CELL PRESS
DOI: 10.1016/j.bpj.2008.11.005
关键词
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类别
资金
- National Institute of Health [R01-HL072011]
- American Heart Association [SDG-0735093N]
Ca2+ transport through mitochondrial Ca2+ uniporter is the primary Ca2+ uptake mechanism in respiring mitochondria. Thus, the uniporter plays a key role in regulating mitochondrial Ca2+. Despite the importance of mitochondrial Ca2+ to metabolic regulation and mitochondrial function, and to cell physiology and pathophysiology, the structure and composition of the uniporter functional unit and kinetic mechanisms associated with Ca2+ transport into mitochondria are still not well understood. In this study, based on available experimental data on the kinetics of Ca2+ transport via the uniporter, a mechanistic kinetic model of the uniporter is introduced. The model is thermodynamically balanced and satisfactorily describes a large number of independent data sets in the literature on initial or pseudo-steady-state influx rates of Ca2+ via the uniporter measured under a wide range of experimental conditions. The model is derived assuming a multi-state catalytic binding and Eyring's free-energy barrier theory-based transformation mechanisms associated with the carrier-mediated facilitated transport and electrodiffusion. The model is a great improvement over the previous theoretical models of mitochondrial Ca2+ uniporter in the literature in that it is thermodynamically balanced and matches a large number of independently published data sets on mitochondrial Ca2+ uptake. This theoretical model will be critical in developing mechanistic, integrated models of mitochondrial Ca2+ handling and bioenergetics which can be helpful in understanding the mechanisms by which Ca2+ plays a role in mediating signaling pathways and modulating mitochondrial energy metabolism.
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