1. Can a single "powerless" mitochondrion in the malaria parasite contribute to parasite programmed cell death in the asexual stages?
- Author
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Ch'ng JH, Yeo SP, and Shyong-Wei Tan K
- Subjects
- Animals, Antimalarials therapeutic use, Artemisinins therapeutic use, Drug Resistance genetics, Humans, Lactones therapeutic use, Malaria, Falciparum drug therapy, Malaria, Falciparum genetics, Malaria, Falciparum pathology, Malaria, Vivax drug therapy, Malaria, Vivax genetics, Malaria, Vivax pathology, Mitochondria genetics, Plasmodium falciparum genetics, Plasmodium vivax genetics, Apoptosis, Malaria, Falciparum metabolism, Malaria, Vivax metabolism, Mitochondria metabolism, Plasmodium falciparum metabolism, Plasmodium vivax metabolism
- Abstract
The protozoan pathogens responsible for malaria are from the Plasmodium genus, with Plasmodium falciparum and Plasmodium vivax accounting for almost all clinical infections. With recent estimates of mortality exceeding 800,000 annually, malaria continues to take a terrible toll on lives and the early promises of medicine to eradicate the disease have yet to approach realization, in part due to the spread of drug resistant parasites. Recent reports of artemisinin-resistance have prompted renewed efforts to identify novel therapeutic options, and one such pathway being considered for antimalarial exploit is the parasite's programmed cell death (PCD) pathway. In this mini-review, we will discuss the roles of the plasmodium mitochondria in cell death and as a target of antimalarial compounds, taking into account recent data suggesting that PCD pathways involving the mitochondria may be attractive antimalarial targets., (Copyright © 2012 Elsevier B.V. and Mitochondria Research Society. All rights reserved.)
- Published
- 2013
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