Mitochondrial fission - a drug target for cytoprotection or cytodestruction?
AuthorRosdah, AA; Holien, JK; Delbridge, LMD; Dusting, GJ; Lim, SY
Source TitlePharmacology Research and Perspectives
PublisherJOHN WILEY & SONS LTD
AffiliationSurgery (St Vincent's)
Document TypeJournal Article
CitationsRosdah, A. A., Holien, J. K., Delbridge, L. M. D., Dusting, G. J. & Lim, S. Y. (2016). Mitochondrial fission - a drug target for cytoprotection or cytodestruction?. PHARMACOLOGY RESEARCH & PERSPECTIVES, 4 (3), https://doi.org/10.1002/prp2.235.
Access StatusOpen Access
Mitochondria are morphologically dynamic organelles constantly undergoing processes of fission and fusion that maintain integrity and bioenergetics of the organelle: these processes are vital for cell survival. Disruption in the balance of mitochondrial fusion and fission is thought to play a role in several pathological conditions including ischemic heart disease. Proteins involved in regulating the processes of mitochondrial fusion and fission are therefore potential targets for pharmacological therapies. Mdivi-1 is a small molecule inhibitor of the mitochondrial fission protein Drp1. Inhibiting mitochondrial fission with Mdivi-1 has proven cytoprotective benefits in several cell types involved in a wide array of cardiovascular injury models. On the other hand, Mdivi-1 can also exert antiproliferative and cytotoxic effects, particularly in hyperproliferative cells. In this review, we discuss these divergent effects of Mdivi-1 on cell survival, as well as the potential and limitations of Mdivi-1 as a therapeutic agent.
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