- Poster presentation
- Open Access
Sex, power and drugs: the murky world of malaria parasite mitochondria
Malaria Journal volume 13, Article number: P11 (2014)
It is hypothesised that intraerythrocytic malaria parasite metabolism is not just fulfilling the need for ATP generation, but is highly evolved to support rapid proliferation, similar to what is seen in other rapidly proliferating cells such as cancer cells. Evidence is presented that deregulated glycolytic activity coupled with impaired mitochondrial metabolism is a metabolic strategy to generate glycolytic intermediates essential for rapid biomass generation for schizogony.
The role of the parasite mitochondrion during key stages of the parasite life cycle makes it an attractive target for the development of novel prophylaxis, treatment and transmission blocking drugs. Using a targeted pharmacometabolomic approach, additional mitochondrial targets with therapeutic potential are identified and the potential of the development of inhibitors against these novel targets is discussed in the context of recent experiences with bc1 and dihydroorotate dehydrogenase-targeting drug development programmes and within the context of current target product profiles for the malaria elimination agenda.
Rights and permissions
This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
About this article
Cite this article
Biagini, G. Sex, power and drugs: the murky world of malaria parasite mitochondria. Malar J 13 (Suppl 1), P11 (2014). https://doi.org/10.1186/1475-2875-13-S1-P11
- Malaria Parasite
- Blocking Drug
- Malaria Elimination
- Mitochondrial Target