Endoplasmic Reticulum-Mitochondria Communication Through Ca2+ Signaling: The Importance of Mitochondria-Associated Membranes (MAMs)

Marchi, Saverio; Bittremieux, Mart; Missiroli, Sonia; Morganti, Claudia; Patergnani, Simone; Sbano, Luigi; Rimessi, Alessandro; Kerkhofs, Martijn; Parys, Jan B.; Bultynck, Geert; Giorgi, Carlotta; Pinton, Paolo

doi:10.1007/978-981-10-4567-7_4

Cited by 111 publications

(82 citation statements)

References 144 publications

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“…Among its many functions, mitochondrial calcium buffering capacity regulates the intracellular concentration of calcium, not only by buffering local changes in the cytosol, but also via highly regulated contacts with the plasma membrane and/or the ER (178,179). Therefore, alterations in the communication between mitochondria and these organelles can significantly impact the entry of calcium into mitochondria, affecting overall calcium signaling in the cell (180,181). Notably, calcium concentration is a regulator of rate-limiting enzymes in the Krebs cycle, and increases in calcium in the mitochondrial matrix activate the Krebs cycle and OxPhos (182).…”

Section: Possible Mechanism Of Oxphos Deficiency In Neurodegenerativementioning

confidence: 99%

Mitochondria, OxPhos, and neurodegeneration: cells are not just running out of gas

Area‐Gómez¹,

Guardia‐Laguarta²,

Schon

et al. 2019

Journal of Clinical Investigation

125

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Section: Possible Mechanism Of Oxphos Deficiency In Neurodegenerativementioning

confidence: 99%

Mitochondria, OxPhos, and neurodegeneration: cells are not just running out of gas

Area‐Gómez¹,

Guardia‐Laguarta²,

Schon

et al. 2019

Journal of Clinical Investigation

125

View full text Add to dashboard Cite

“…This effect may be because of changes in the redox environment and thus in the redox state of IP 3 R1 (Joseph et al 2018). There is thus an intricate cross talk between Ca 2+ signals, ROS production, and mPTP opening, which is frequently dysregulated in severe human pathologies such as cardiovascular diseases, cancer, and neurodegeneration (Feissner et al 2009;Marchi et al 2017).…”

Section: Mitochondrial Permeability Transition Porementioning

confidence: 99%

Cytoplasmic and Mitochondrial Calcium Signaling: A Two-Way Relationship

Wacquier

Combettes

Dupont

2019

Cold Spring Harb Perspect Biol

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Intracellular Ca 2+ signals are well organized in all cell types, and trigger a variety of vital physiological processes. The temporal and spatial characteristics of cytosolic Ca 2+ increases are mainly governed by the fluxes of this ion across the membrane of the endoplasmic/sarcoplasmic reticulum and the plasma membrane. However, various Ca 2+ transporters also allow for Ca 2+ exchanges between the cytoplasm and mitochondria. Increases in mitochondrial Ca 2+ stimulate the production of ATP, which allows the cells to cope with the increased energy demand created by the stimulus. Less widely appreciated is the fact that Ca 2+ handling by mitochondria also shapes cytosolic Ca 2+ signals. Indeed, the frequency, amplitude, and duration of cytosolic Ca 2+ increases can be altered by modifying the rates of Ca 2+ transport into, or from, mitochondria. In this review, we focus on the interplay between mitochondria and Ca 2+ signaling, highlighting not only the consequences of cytosolic Ca 2+ changes on mitochondrial Ca 2+ , but also how cytosolic Ca 2+ dynamics is controlled by modifications of the Ca 2+ -handling properties and the metabolism of mitochondria.

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“…The close proximity between mitochondria and a subdomain of the ER, termed the mitochondria‐associated membrane (MAM; Paillusson et al , ; Herrera‐Cruz & Simmen, ), allows efficient Ca 2+ transfer from the ER to mitochondria. Uptake of Ca 2+ into the matrix of mitochondria activates the tricarboxylic acid cycle, leading to the production of ATP, whereas prolonged excess Ca 2+ uptake results in the release of apoptosis‐inducing factors from mitochondria (Herrera‐Cruz & Simmen, ; Marchi et al , ). Mitochondria generate ATP via the proton gradient across the mitochondrial inner membrane that is formed as a consequence of the passage of electrons through the electron transport chain.…”

Section: Introductionmentioning

confidence: 99%

Syntaxin 17 regulates the localization and function of PGAM5 in mitochondrial division and mitophagy

et al. 2018

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PGAM5, a mitochondrial protein phosphatase that is genetically and biochemically linked to PINK1, facilitates mitochondrial division by dephosphorylating the mitochondrial fission factor Drp1. At the onset of mitophagy, PGAM5 is cleaved by PARL, a rhomboid protease that degrades PINK1 in healthy cells, and the cleaved form facilitates the engulfment of damaged mitochondria by autophagosomes by dephosphorylating the mitophagy receptor FUNDC1. Here, we show that the function and localization of PGAM5 are regulated by syntaxin 17 (Stx17), a mitochondria-associated membrane/mitochondria protein implicated in mitochondrial dynamics in fed cells and autophagy in starved cells. In healthy cells, loss of Stx17 causes PGAM5 aggregation within mitochondria and thereby failure of the dephosphorylation of Drp1, leading to mitochondrial elongation. In Parkin-mediated mitophagy, Stx17 is prerequisite for PGAM5 to interact with FUNDC1. Our results reveal that the Stx17-PGAM5 axis plays pivotal roles in mitochondrial division and PINK1/Parkin-mediated mitophagy.

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Endoplasmic Reticulum-Mitochondria Communication Through Ca2+ Signaling: The Importance of Mitochondria-Associated Membranes (MAMs)

Cited by 111 publications

References 144 publications

Mitochondria, OxPhos, and neurodegeneration: cells are not just running out of gas

Mitochondria, OxPhos, and neurodegeneration: cells are not just running out of gas

Cytoplasmic and Mitochondrial Calcium Signaling: A Two-Way Relationship

Syntaxin 17 regulates the localization and function of PGAM5 in mitochondrial division and mitophagy

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