Abstract
Stimulation of mitochondrial oxidative metabolism by Ca2+ is now generally recognised as important for the control of cellular ATP homeostasis. Here, we review the mechanisms through which Ca2+ regulates mitochondrial ATP synthesis. We focus on cardiac myocytes and pancreatic β-cells, where tight control of this process is likely to play an important role in the response to rapid changes in workload and to nutrient stimulation, respectively. We also describe a novel approach for imaging the Ca2+-dependent regulation of ATP levels dynamically in single cells.
| Original language | English |
|---|---|
| Pages (from-to) | 28-35 |
| Number of pages | 8 |
| Journal | Cell Calcium |
| Volume | 52 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published (in print/issue) - Jul 2012 |
Funding
GAR and AIT thank the Royal Society and the Juvenile Diabetes Research Foundation respectively for a Wolfson Research Merit Award and a post-doctoral Fellowship. Work in GAR's laboratory is supported by the Wellcome Trust (Programme 081958/Z/07/Z ), DiabetesUK (Project 11/0004210) and the European Association for the Study of Diabetes (EFSD) . EJG was supported by the British Heart Foundation , the Biotechnology and Biological Sciences Research Council , and the Medical Research Council (U.K.) . We would like to thank Professor Richard M. Denton (University of Bristol) for critical comments on the text.
Keywords
- ATP
- Beta cell
- Calcium
- Diabetes
- Heart
- Insulin
- Islet
- Mitochondria
- Secretion
