The Role of Mitochondria in Cytoplasmic Ca²⁺ Cycling

Abstract

It has been known for a long time that isolated mitochondria are able to accumulate large amounts of calcium ions. Before the discovery that endoplasmic reticulum (ER) was the main Ca2+‐storing cellular organelle, mitochondria were thought to play a major role in cytoplasmic Ca2+ homeostasis (Carafoli, 2002). After IP3 was discovered and it was shown that IP3 receptors were localized in ER membrane and that Ca2+‐binding proteins such as calsequestrin could store large amounts of Ca2+ in the ER, the role of mitochondria in the regulation of cytoplasmic Ca2+ was questioned. However, in recent years, mostly due to the development of new methods, there has been increasing evidence that mitochondria could be an important cytoplasmic Ca2+ sink, especially under conditions of a high cellular Ca2+ load.

WldS Prevents Axon Degeneration through Increased Mitochondrial Flux and Enhanced Mitochondrial Ca2+ Buffering

“…This would be consistent with the observation that blocking Ca 2+ channels inhibits Wallerian degeneration [10, 18]. Mitochondria are a well-established sink for Ca 2+ in axons [14] and here we show that Wld s+ mitochondria exhibit enhanced Ca 2+ buffering capacity and resistance to Ca 2+ -induced formation of the permeability transition pore (PTP). Indeed PTP formation appears to be a key final execution step in Wallerian degeneration [20–22].…”

“…Mitochondria are major sinks for cellular Ca 2+ in both axons and synapses [14]. A powerful mechanism by which Wld S could exert all of these effects would be by altering mitochondrial Ca 2+ buffering capacity.…”

Critical illness myopathy: what is happening?

“…Reactive oxygen species released from dysfunctional mitochondria or by TNF-a-mediated cyclooxygenase pathway stimulation also have deleterious effects on the sarcoplasmic reticulum, myofilaments and sarcolemmal proteins [46]. Moreover, the opening of mitochondrial transition pores [69] and subsequent release of cytochrome C act as proapoptotic signals. Other possible metabolic pathways for muscle damage (usually seen in other contexts not related to critical illness) may involve protein kinases [70], defensins and cathelicidins [71,72] or hypogonadism [73], which have not been elucidated so far for CIM.…”

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“…ùóºòüñÿ ÷óòëèâ³ñòü ÌÏ äî 䳿 Ñà 2+ ÿê ïðè ô³ç³îëîã³÷í³é êîíöåíòðàö³¿, òàê ³ çà óìîâ éîãî íàâàíòàaeåííÿ. Öå, éìîâ³ðíî, ïîâÿçàíî ç ïîðóøåííÿì êàëüö³ºâîãî ãîìåî ñòàçó, â îñíîâ³ ÿêîãî º çì³íà êîíöåíòðàö³¿ Ñà 2+ , ïðîöåñ³â éîãî êë³òèííîãî äåïîíóâàííÿ òà ìîäèô³êàö³ÿ ìåìáðàííî¿ ïðîíèêíîñò³ äëÿ öèõ ³îí³â [2,15,17]. Àêòèâàö³ÿ ÌÏ êàëüö³ºì â³äáóâàºòüñÿ íàñàìïåðåä âíàñë³äîê ïðèãí³-÷åííÿ îêèñíîãî ôîñôîðèëþâàííÿ, ïîâÿçàí-íîãî ç ïîñèëåííÿì ãåíåðàö³¿ ì³òîõîíäð³ÿìè â³ëüíèõ ðàäèêàë³â [16,18].…”