The execution of proper Ca2+ signaling requires close apposition between the endoplasmic reticulum (ER) and mitochondria. Hence, Ca2+ released from the ER is “quasi-synaptically” transferred to mitochondrial matrix, where Ca2+ stimulates mitochondrial ATP synthesis by activating the tricarboxylic acid (TCA) cycle. However, when the Ca2+ transfer is excessive and sustained, mitochondrial Ca2+ overload induces apoptosis by opening the mitochondrial permeability transition pore. A large number of regulatory proteins reside at mitochondria-associated ER membranes (MAMs) to maintain the optimal distance between the organelles and to coordinate the functionality of both ER and mitochondrial Ca2+ transporters or channels. In this chapter, we discuss the different pathways involved in the regulation of ER-mitochondria Ca2+ flux and describe the activities of the various Ca2+ players based on their primary intra-organelle localization.

Endoplasmic reticulum-mitochondria communication through Ca2+ signaling: The importance of mitochondria-associated membranes (MAMs)

Marchi, Saverio;Missiroli, Sonia;Morganti, Claudia;Patergnani, Simone;Sbano, Luigi;Rimessi, Alessandro;Giorgi, Carlotta;Pinton, Paolo
2017

Abstract

The execution of proper Ca2+ signaling requires close apposition between the endoplasmic reticulum (ER) and mitochondria. Hence, Ca2+ released from the ER is “quasi-synaptically” transferred to mitochondrial matrix, where Ca2+ stimulates mitochondrial ATP synthesis by activating the tricarboxylic acid (TCA) cycle. However, when the Ca2+ transfer is excessive and sustained, mitochondrial Ca2+ overload induces apoptosis by opening the mitochondrial permeability transition pore. A large number of regulatory proteins reside at mitochondria-associated ER membranes (MAMs) to maintain the optimal distance between the organelles and to coordinate the functionality of both ER and mitochondrial Ca2+ transporters or channels. In this chapter, we discuss the different pathways involved in the regulation of ER-mitochondria Ca2+ flux and describe the activities of the various Ca2+ players based on their primary intra-organelle localization.
2017
978-981-10-4566-0
978-981-10-4567-7
Apoptosis; Autophagy; Calcium; Cell death; Endoplasmic reticulum (ER); ER-mitochondria contact sites; Mitochondria; Mitochondria associated membranes (MAMs); ROS; Animals; Apoptosis; Endoplasmic Reticulum; Energy Metabolism; Humans; Membrane Microdomains; Membrane Proteins; Mitochondria; Mitochondrial Membrane Transport Proteins; Mitochondrial Membranes; Mitochondrial Proteins; Calcium Signaling; Biochemistry, Genetics and Molecular Biology (all)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11392/2382180
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