Toll‐like receptors hit calcium |
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| Authors: | Marina de Bernard Rosario Rizzuto |
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| Affiliation: | 1. Department of Biology, University of Padova, Padova, Italy;2. Department of Biomedical Sciences, CNR Neuroscience Institute, University of Padova, Padova, Italy |
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| Abstract: | Mitochondrial Ca2+ uptake is a multifarious signal that controls both the activity of matrix dehydrogenases and the sensitivity to apoptotic and necrotic challenges. Recent evidence indicates that mitochondria also play a role in triggering inflammation, as mitochondrial DNA, when released by the cell, is an important damage‐associated molecular pattern (DAMP). Now, Toll‐like receptors (TLRs) are shown to close the loop, by affecting in turn mitochondrial activity. Two studies by Shintani and colleagues, one in this issue of EMBO reports 1 2 , identify a new TLR transduction mechanism that impinges directly on mitochondrial function. Upon binding of CpG oligodeoxynucleotides, TLR9—which in non‐immune cells is retained in the ER—inhibits SERCA2, thus reducing Ca2+ transfer to the mitochondria and aerobic metabolism. |
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