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Elusive mitochondrial connection to inflammation uncovered

PINK1 and parkin proteins help to degrade damaged mitochondrial organelles, and abnormalities in these proteins are linked to Parkinson’s disease. Mouse studies reveal that the proteins act to prevent inflammation.
  1. Alexandra Stolz

    1. Alexandra Stolz is in the Institute of Biochemistry II and Buchmann Institute for Molecular Life Sciences, Goethe University School of Medicine, 60590 Frankfurt am Main, Germany.

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  2. Ivan Dikic

    1. Ivan Dikic is in the Institute of Biochemistry II and Buchmann Institute for Molecular Life Sciences, Goethe University School of Medicine, 60590 Frankfurt am Main, Germany.

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Neurodegenerative conditions such as Parkinson’s and Alzheimer’s diseases constitute a major human-health burden. Although the symptoms, or the cells affected, can differ in such disorders, some neurodegenerative diseases have certain characteristics in common. These include a state of inflammation1 and impaired elimination of defective mitochondrial organelles2. However, it remains to be determined whether such common alterations are interconnected, and whether they are a cause or a consequence of disease. Writing in Nature, Sliter et al.3 report their investigation of mice that have alterations in genes linked to Parkinson’s disease. The authors identify a direct connection between the cellular process that eliminates damaged mitochondria — called mitophagy — and inflammation.

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Nature 561, 185-186 (2018)

doi: https://doi.org/10.1038/d41586-018-05988-z

References

  1. Glass, C. K., Saijo, K., Winner, B., Marchetto, M. C. & Gage, F. H. Cell 140, 918–934 (2010).

    Article  PubMed  Google Scholar 

  2. Burté, F., Carelli, V., Chinnery, P. F. & Yu-Wai-Man, P. Nature Rev. Neurol. 11, 11–24 (2015).

    Article  PubMed  Google Scholar 

  3. Sliter, D. A. et al. Nature 561, 258–262 (2018).

    Article  Google Scholar 

  4. Harper, J. W., Ordureau, A. & Heo, J. M. Nature Rev. Mol. Cell Biol. 19, 93–108 (2018).

    Article  PubMed  Google Scholar 

  5. Pickrell, A. M. & Youle, R. J. Neuron 85, 257–273 (2015).

    Article  PubMed  Google Scholar 

  6. Scarffe, L. A., Stevens, D. A., Dawson, V. L. & Dawson, T. M. Trends Neurosci. 37, 315–324 (2014).

    Article  PubMed  Google Scholar 

  7. Yan, M. H, Wang, X. & Zhu, X. Free Radic. Biol. Med. 62, 90–101 (2013).

    Article  PubMed  Google Scholar 

  8. Rongvaux, A. et al. Cell 159, 1563–1577 (2014).

    Article  PubMed  Google Scholar 

  9. White, M. J. et al. Cell 159, 1549–1562 (2014).

    Article  PubMed  Google Scholar 

  10. Pickrell, A. M. et al. Neuron 87, 371–381 (2015).

    Article  PubMed  Google Scholar 

  11. Noyce, A. J. et al. Ann. Neurol. 72, 893–901 (2012).

    Article  PubMed  Google Scholar 

Download references

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