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Mitochondrial calcium homeostasis as potential target for mitochondrial medicine

期刊

MITOCHONDRION
卷 12, 期 1, 页码 77-85

出版社

ELSEVIER SCI LTD
DOI: 10.1016/j.mito.2011.07.004

关键词

Mitochondria; Calcium; Aging; Neurodegeneration; Diabetes; Cardiovascular and mitochondrial disorders

资金

  1. Ministry of Science and Higher Education, Poland [NN407 075 137]
  2. Italian Association for Cancer Research (AIRC), Telethon [GGP09128]
  3. University of Ferrara
  4. Italian Ministry of Education
  5. University and Research (COFIN)
  6. Italian Cystic Fibrosis Research Foundation
  7. Italian Ministry of Health
  8. FIRC
  9. FISM - Fondazione Italiana Sclerosi Multipla [Cod. 2010/B/1, Cod. 2010/B/13]
  10. Foundation for Polish Science (FNP)
  11. UE
  12. European Regional Development Fund
  13. Operational Programme Innovative Economy

向作者/读者索取更多资源

Mitochondria are crucial in different intracellular pathways of signal transduction. Mitochondria are capable of decoding a variety of extracellular stimuli into markedly different intracellular actions, ranging from energy production to cell death. The fine modulation of mitochondrial calcium (Ca2+) homeostasis plays a fundamental role in many of the processes involving this organelle. When mitochondrial Ca2+ homeostasis is compromised, different pathological conditions can occur, depending on the cell type involved. Recent data have shed light on the molecular identity of the main proteins involved in the handling of mitochondrial Ca2+ traffic, opening fascinating and ambitious new avenues for mitochondria-based pharmacological strategies. (C) 2011 Elsevier B.V. and Mitochondria Research Society. All rights reserved.

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