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.

Mitochondrial calcium homeostasis as potential target for mitochondrial medicine

GIORGI, Carlotta
Primo
;
AGNOLETTO, Chiara
Secondo
;
BONONI, Angela;BONORA, Massimo;DE MARCHI, Elena;MARCHI, Saverio;MISSIROLI, Sonia;PATERGNANI, Simone;POLETTI, Federica;RIMESSI, Alessandro;PINTON, Paolo
Ultimo
2012

Abstract

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.
2012
Giorgi, Carlotta; Agnoletto, Chiara; Bononi, Angela; Bonora, Massimo; DE MARCHI, Elena; Marchi, Saverio; Missiroli, Sonia; Patergnani, Simone; Poletti, Federica; Rimessi, Alessandro; Suski, Jm; Wieckowski, M; Pinton, Paolo
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/1466713
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