Journal
CELL CALCIUM
Volume 69, Issue -, Pages 73-80Publisher
ELSEVIER SCI LTD
DOI: 10.1016/j.ceca.2017.08.008
Keywords
Mitochondria; Calcium; Cell death; MCU; MCU complex
Categories
Funding
- University of Padova
- Italian Ministries of Health (Ricerca Finalizzata)
- Education, University and Research (FIRB)
- European Union (ERC mitoCalcium) [294777]
- NIH [1P01AG025532-01A1]
- Cariparo Foundation
- Italian Association for Cancer Research
- AIRC
- Telethon-Italy [GPP1005A]
- Junta de Extremadura - European Regional Development Fund, ERDF [PO14011]
- NATIONAL INSTITUTE ON AGING [P01AG025532] Funding Source: NIH RePORTER
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During the 60s, the notion that positively charged Ca2+ ions are rapidly accumulated in energized mitochondria has been first established. In the following decades, mitochondrial Ca2+ homeostasis was shown to control cell metabolism, cell survival and other cell-specific functions through different mechanism. However, the molecular identity of the molecules controlling this process remained a mystery until just few years ago, when both mitochondrial Ca2+ uptake and release systems were genetically dissected. This finally opened the possibility to develop genetic model to directly test the contribution of mitochondrial Ca2+ homeostasis to cellular functions. Although the picture is still far from being clear, we here summarize and critically evaluate the current knowledge on how mitochondrial Ca2+ handling controls cell death.
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