A dismaying update: the paper in question contains a significant amount of outright plagiarism, and large chunks of text are taken literally from Butterﬁeld et al. 2006, “Oxidative stress in
Alzheimer’s disease brain: New insights from
redox proteomics,” European Journal of
Pharmacology 545: 39-50. I hope we hear from Han and Warda sometime; they've got a lot of 'splaining to do.
Mitochondria are fascinating organelles. They are the "powerhouses of the cell" (that phrase is required to be used in any discussion of their function) that generate small, energy rich molecules like ATP that are used in many cellular chemical reactions, but they also have important roles in cell signaling and cell death. They also have a peculiar evolutionary history, arising as endosymbionts; their ancestors were independent organisms that took up residence inside eukaryotic cells in a mutually happy and long-lasting relationship. They exhibit some interesting relics of that prior history, as mitochondria have their own private strand of DNA which encodes some of the genes needed for the chemical processes they execute. Other genes for those functions have migrated over evolutionary time into the nuclear genome, which means the mix of gene products operating in the organelle are from two sources, the mitochondrial and nuclear genome. It's a good subject for studies in proteomics.
Right now, there is a paper that is available as an Epub ahead of print in the journal Proteomics. It is not promising. In fact, all you have to do is read the title to make you wonder what the authors, Warda and Han, were smoking: "Mitochondria, the missing link between body and soul: Proteomic prospective evidence."
Attila Csordas asks, "Can you tell a good article from a bad based on the abstract and the title alone?", and I'm inclined to say yes. Sometimes you get pleasant surprises in the full paper that were not well described in the abstract, but when the abstract and title contain hints that the bridge is out and that somebody has switched the train to the wrong tracks, you can predict that there will be a train wreck if you read further. Here's the abstract. I've highlighted one provocative statement.
Mitochondria are the gatekeepers of the life and death of most cells that regulate signaling, metabolism, and energy production needed for cellular function. Therefore, unraveling of the genuine mitochondrial proteome, as the dynamic determinant of structural-functional integrity to the cellular framework, affords a better understanding of many still-hidden secrets of life behind the already known static genome. Given the critical mitochondrial role under different stress conditions, the aim of the current review is to merge the available scientific data related to mitochondrial proteomes and frame them into a reliable new agreement extending beyond the limited already accepted endosymbiotic hypothesis into broader fundamental mechanisms orchestrating cellular outcome on behalf of cell survival. The focus of this work is to cover first the mitochondrial proteome/genome interplay that is currently believed to be implicated in a range of human diseases. The mechanochemical coupling between mitochondria and different cytoskeleton proteins and the impact of the mitoskeleton on mitochondrial structure and function are then addressed. Further crosstalk between mitochondria and other cellular organelles, e.g., the ER and the nucleus is then discussed. Additionally, the role of mitochondria in apoptosis and the mitochondrial contribution in intercellular communication mediated by gap junctions are also described. These data are presented with other novel proteomics evidence to disprove the endosymbiotic hypothesis of mitochondrial evolution that is replaced in this work by a more realistic alternative. Furthermore, the role of mitochondria in development of oxidative stress-based diseases, e.g., neurodegenerative and cardiovascular diseases is pointed out together with the prospective proteomics view as an alternative prognostic and diagnostic tool for interpreting many mitochondria-related anomalies. The insights generated by recent proteomic research that provide a rational impact on possible mitochondrial-targeted therapeutic interventions are also discussed.
My blog makes a career out of describing train wrecks, so how could I not continue on and read the paper?
Continue reading "A baffling failure of peer review" (on Pharyngula)