Mitochondrial Ca²⁺ and apoptosis

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• 作者：Carlotta Giorgi ; Federica Baldassari ; Angela Bononi ; Massimo Bonora ; Elena De Marchi ; Saverio Marchi ; Sonia Missiroli ; Simone Patergnani ; Aless ; ro Rimessi ; Jan M. Suski ; Mariusz R. Wieckowski ; Paolo Pinton
• 关键词：Calcium ; Mitochondria ; Apoptosis ; Cell death ; Endoplasmic reticulum ; MAM
• 刊名：Cell Calcium
• 出版年：2012
• 出版时间：July, 2012
• 年：2012
• 卷：52
• 期：1
• 页码：36-43
• 全文大小：521 K

文摘

Mitochondria are key decoding stations of the apoptotic process. In support of this view, a large body of experimental evidence has unambiguously revealed that, in addition to the well-established function of producing most of the cellular ATP, mitochondria play a fundamental role in triggering apoptotic cell death.

Various apoptotic stimuli cause the release of specific mitochondrial pro-apoptotic factors into the cytosol. The molecular mechanism of this release is still controversial, but there is no doubt that mitochondrial calcium (Ca²⁺) overload is one of the pro-apoptotic ways to induce the swelling of mitochondria, with perturbation or rupture of the outer membrane, and in turn the release of mitochondrial apoptotic factors into the cytosol.

Here, we review as different proteins that participate in mitochondrial Ca²⁺ homeostasis and in turn modulate the effectiveness of Ca²⁺-dependent apoptotic stimuli. Strikingly, the final outcome at the cellular level is similar, albeit through completely different molecular mechanisms: a reduced mitochondrial Ca²⁺ overload upon pro-apoptotic stimuli that dramatically blunts the apoptotic response.