Here are two good recent articles which discuss RSV, AiCAR, Bezafibrate
, rapamycin and other compounds:
Pharmacological approaches to restore mitochondrial function Nature Reviews Drug Discovery 12, 465–483 (2013)
Mitochondrial dysfunction is not only a hallmark of rare inherited mitochondrial disorders but also implicated in age-related diseases, including those that affect the metabolic and nervous system, such as type 2 diabetes and Parkinson's disease. Numerous pathways maintain and/or restore proper mitochondrial function, including mitochondrial biogenesis, mitochondrial dynamics, mitophagy and the mitochondrial unfolded protein response. New and powerful phenotypic assays in cell-based models as well as multicellular organisms have been developed to explore these different aspects of mitochondrial function. Modulating mitochondrial function has therefore emerged as an attractive therapeutic strategy for several diseases, which has spurred active drug discovery efforts in this area.
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Br J Pharmacol. 2013 Sep 18. doi: 10.1111/bph.12413. [Epub ahead of print]
Turn up the power - pharmacological activation of mitochondrial biogenesis in mouse models.Komen JC,
Thorburn DR. Murdoch Childrens Research Institute, Royal Children's Hospital, Flemington Road, Parkville, VIC 3052, Australia.
Abstract The oxidative phosphorylation (OXPHOS) system in mitochondria is responsible for the generation of the majority of cellular energy in the form of ATP. Patients with genetic OXPHOS disorders form the largest group of inborn errors of metabolism. Unfortunately, there is still a lack of efficient therapies for these disorders other than management of symptoms. Developing therapies has been complicated because, although the total group of OXPHOS patients is relatively large, there is enormous clinical and genetic heterogeneity within this patient population. Thus there has been a lot of interest in generating relevant mouse models for the different kinds of OXPHOS disorders. The most common treatment strategies tested in these mouse models have aimed to upregulate mitochondrial biogenesis, with the rationale of increasing the residual OXPHOS activity present in affected animals and thereby ameliorating the energy deficiency. Drugs such as bezafibrate, resveratrol and AICAR target the master regulator of mitochondrial biogenesis PGC-1α either directly or indirectly to manipulate mitochondrial metabolism. This review will summarize the outcome of pre-clinical treatment trials with these drugs in mouse models of OXPHOS disorders and discuss similar treatments in a number of mouse models of common diseases in which pathology is closely linked to mitochondrial dysfunction. In the majority of these studies the pharmacological activation of the PGC-1α axis shows true potential as therapy, however other effects besides mitochondrial biogenesis may be contributing to this as well. This article is protected by copyright. All rights reserved.
KEYWORDS: AICAR, PGC-1α, bezafibrate, mitochondria, mitochondrial biogenesis, mitochondrial disease, mouse models, oxidative phosphorylation, resveratrol
PMID: 24102298
Figure 1 in the 1st paper is especially helpful as it shows most of the compounds and their sites of action:
LongeCity
