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Science China Life Sciences

, Volume 54, Issue 8, pp 763–769

First Online: 24 July 2011Received: 06 June 2011Accepted: 27 June 2011

Abstract

Intracellular Ca is vital for cell physiology. Disruption of Ca homeostasis contributes to human diseases such as heart failure, neuron-degeneration, and diabetes. To ensure an effective intracellular Ca dynamics, various Ca transport proteins localized in different cellular regions have to work in coordination. The central role of mitochondrial Ca transport mechanisms in responding to physiological Ca pulses in cytosol is to take up Ca for regulating energy production and shaping the amplitude and duration of Ca transients in various micro-domains. Since the discovery that isolated mitochondria can take up large quantities of Ca approximately 5 decades ago, extensive studies have been focused on the functional characterization and implication of ion channels that dictate Ca transport across the inner mitochondrial membrane. The mitochondrial Ca uptake sensitive to non-specific inhibitors ruthenium red and Ru360 has long been considered as the activity of mitochondrial Ca uniporter MCU. The general consensus is that MCU is dominantly or exclusively responsible for the mitochondrial Ca influx. Since multiple Ca influx mechanisms e.g. L-, T-, and N-type Ca channel have their unique functions in the plasma membrane, it is plausible that mitochondrial inner membrane has more than just MCU to decode complex intracellular Ca signaling in various cell types. During the last decade, four molecular identities related to mitochondrial Ca influx mechanisms have been identified. These are mitochondrial ryanodine receptor, mitochondrial uncoupling proteins, LETM1 Ca-H exchanger, and MCU and its Ca sensing regulatory subunit MICU1. Here, we briefly review recent progress in these and other reported mitochondrial Ca influx pathways and their differences in kinetics, Ca dependence, and pharmacological characteristics. Their potential physiological and pathological implications are also discussed.

Keywordsmitochondrial calcium channels calcium transport mitochondria heart ryanodine receptor This article is published with open access at Springerlink.com

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Autor: Shi Pan - Shin-Young Ryu - Shey-Shing Sheu

Fuente: https://link.springer.com/article/10.1007/s11427-011-4203-9







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