Mitochondrial Stress Signalling: HTRA2 and Parkinson's Disease
Mitochondria are cellular energy generators whose activity requires a continuous supply of oxygen. Recent genetic analysis has suggested that defects in mitochondrial quality control may be key factors in the development of Parkinson’s disease (PD). Mitochondria have a crucial role in supplying ener...
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| Format: | Article |
| Language: | English |
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Wiley
2012-01-01
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| Series: | International Journal of Cell Biology |
| Online Access: | http://dx.doi.org/10.1155/2012/607929 |
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| author | Enrico Desideri L. Miguel Martins |
| author_facet | Enrico Desideri L. Miguel Martins |
| author_sort | Enrico Desideri |
| collection | DOAJ |
| description | Mitochondria are cellular energy generators whose activity requires a continuous supply of oxygen. Recent genetic analysis has suggested that defects in mitochondrial quality control may be key factors in the development of Parkinson’s disease (PD). Mitochondria have a crucial role in supplying energy to the brain, and their deterioration can affect the function and viability of neurons, contributing to neurodegeneration. These organelles can sow the seeds of their own demise because they generate damaging oxygen-free radicals as a byproduct of their intrinsic physiological functions. Mitochondria have therefore evolved specific molecular quality control mechanisms to compensate for the action of damaging agents such as oxygen-free radicals. PTEN-induced putative kinase 1 (PINK1) and high-temperature-regulated A2 (HTRA2), a mitochondrial protease, have recently been proposed to be key modulators of mitochondrial molecular quality control. Here, we review some of the most recent advances in our understanding of mitochondria stress-control pathways, focusing on how signalling by the p38 stress kinase pathway may regulate mitochondrial stress by modulating the activity of HTRA2 via PINK1 and cyclin-dependent kinase 5 (CDK5). We also propose how defects in this pathway may contribute to PD. |
| format | Article |
| id | doaj-art-175c861558044875801c942b09ad51a4 |
| institution | Kabale University |
| issn | 1687-8876 1687-8884 |
| language | English |
| publishDate | 2012-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | International Journal of Cell Biology |
| spelling | doaj-art-175c861558044875801c942b09ad51a42025-02-03T06:44:37ZengWileyInternational Journal of Cell Biology1687-88761687-88842012-01-01201210.1155/2012/607929607929Mitochondrial Stress Signalling: HTRA2 and Parkinson's DiseaseEnrico Desideri0L. Miguel Martins1Department of Biology, University of Rome “Tor Vergata”, 00133 Rome, ItalyCell Death Regulation Laboratory, MRC Toxicology Unit, Hodgkin Building, Lancaster Road, Leicester LE1 9HN, UKMitochondria are cellular energy generators whose activity requires a continuous supply of oxygen. Recent genetic analysis has suggested that defects in mitochondrial quality control may be key factors in the development of Parkinson’s disease (PD). Mitochondria have a crucial role in supplying energy to the brain, and their deterioration can affect the function and viability of neurons, contributing to neurodegeneration. These organelles can sow the seeds of their own demise because they generate damaging oxygen-free radicals as a byproduct of their intrinsic physiological functions. Mitochondria have therefore evolved specific molecular quality control mechanisms to compensate for the action of damaging agents such as oxygen-free radicals. PTEN-induced putative kinase 1 (PINK1) and high-temperature-regulated A2 (HTRA2), a mitochondrial protease, have recently been proposed to be key modulators of mitochondrial molecular quality control. Here, we review some of the most recent advances in our understanding of mitochondria stress-control pathways, focusing on how signalling by the p38 stress kinase pathway may regulate mitochondrial stress by modulating the activity of HTRA2 via PINK1 and cyclin-dependent kinase 5 (CDK5). We also propose how defects in this pathway may contribute to PD.http://dx.doi.org/10.1155/2012/607929 |
| spellingShingle | Enrico Desideri L. Miguel Martins Mitochondrial Stress Signalling: HTRA2 and Parkinson's Disease International Journal of Cell Biology |
| title | Mitochondrial Stress Signalling: HTRA2 and Parkinson's Disease |
| title_full | Mitochondrial Stress Signalling: HTRA2 and Parkinson's Disease |
| title_fullStr | Mitochondrial Stress Signalling: HTRA2 and Parkinson's Disease |
| title_full_unstemmed | Mitochondrial Stress Signalling: HTRA2 and Parkinson's Disease |
| title_short | Mitochondrial Stress Signalling: HTRA2 and Parkinson's Disease |
| title_sort | mitochondrial stress signalling htra2 and parkinson s disease |
| url | http://dx.doi.org/10.1155/2012/607929 |
| work_keys_str_mv | AT enricodesideri mitochondrialstresssignallinghtra2andparkinsonsdisease AT lmiguelmartins mitochondrialstresssignallinghtra2andparkinsonsdisease |