Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz

Logo MUG-Forschungsportal

Gewählte Publikation:

SHR Neuro Krebs Kardio Lipid

Graier, WF; Frieden, M; Malli, R.
Mitochondria and Ca(2+) signaling: old guests, new functions.
Pflugers Arch. 2007; 455(3): 375-396. [OPEN ACCESS]
Web of Science PubMed FullText FullText_MUG


Autor/innen der Med Uni Graz:
Graier Wolfgang
Malli Roland

Dimensions Citations:

Plum Analytics:

Scite (citation analytics):

Number of Figures: 6
| | | | | |
Mitochondria are ancient endosymbiotic guests that joined the cells in the evolution of complex life. While the unique ability of mitochondria to produce adenosine triphosphate (ATP) and their contribution to cellular nutrition metabolism received condign attention, our understanding of the organelle's contribution to Ca(2+) homeostasis was restricted to serve as passive Ca(2+) sinks that accumulate Ca(2+) along the organelle's negative membrane potential. This paradigm has changed radically. Nowadays, mitochondria are known to respond to environmental Ca(2+) and to contribute actively to the regulation of spatial and temporal patterns of intracellular Ca(2+) signaling. Accordingly, mitochondria contribute to many signal transduction pathways and are actively involved in the maintenance of capacitative Ca(2+) entry, the accomplishment of Ca(2+) refilling of the endoplasmic reticulum and Ca(2+)-dependent protein folding. Mitochondrial Ca(2+) homeostasis is complex and regulated by numerous, so far, genetically unidentified Ca(2+) channels, pumps and exchangers that concertedly accomplish the organelle's Ca(2+) demand. Notably, mitochondrial Ca(2+) homeostasis and functions are crucially influenced by the organelle's structural organization and motility that, in turn, is controlled by matrix/cytosolic Ca(2+). This review intends to provide a condensed overview on the molecular mechanisms of mitochondrial Ca(2+) homeostasis (uptake, buffering and storage, extrusion), its modulation by other ions, kinases and small molecules, and its contribution to cellular processes as fundamental basis for the organelle's contribution to signaling pathways. Hence, emphasis is given to the structure-to-function and mobility-to-function relationship of the mitochondria and, thereby, bridging our most recent knowledge on mitochondria with the best-established mitochondrial function: metabolism and ATP production.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Calcium - metabolism
Calcium Channels - drug effects
Calcium Signaling - physiology
Cell Membrane - physiology
Cytosol - physiology
Endoplasmic Reticulum - physiology
Homeostasis - physiology
Humans -
Ion Channels - physiology
Membrane Potential, Mitochondrial - physiology
Mitochondria - physiology
Mitochondrial Membranes - physiology
Mitochondrial Proteins - physiology
Phosphoproteins - metabolism
Protein Folding -
Reactive Oxygen Species - metabolism
Second Messenger Systems - physiology

Find related publications in this database (Keywords)
mitochondrial Ca2+
mitochondrial Ca2+ uniporter
mitochondrial ion transporters
store operated Ca2+ entry
uncoupling proteins
ER refilling
mitochondrial structure
© Med Uni Graz Impressum