Mitochondrial damage is often both the cause and outcome of cell injury resulting from a variety of toxic insults, hypoxia or trauma. Increasing mitochondrial biogenesis following renal proximal tubular cell (RPTC) injury accelerated the recovery of mitochondrial and cellular functions (Rasbach and Schnellmann, 2007a). However, few pharmacological agents are known to increase mitochondrial biogenesis......
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Daidzein and formononetin induced the expression of SIRT1 in RPTC and the activation of recombinant SIRT1 while DCHC and 7-C only induced the activation of recombinant SIRT1. In contrast, genistein, biochanin A, 4',7-D, and 5,7,4'-T only increased SIRT1 expression in RPTC. We have identified a series of substituted isoflavones that produce mitochondrial biogenesis through PGC-1alpha and increased SIRT1 activity and/or expression, independent of the estrogen receptor. Furthermore, different structural components are responsible for the activities of isoflavones:
- the hydroxyl group at position 7 is required SIRT1 activation
- A hydroxyl group at position 5 blocks SIRT1 activation
- the loss of the phenyl ring at position 3 or the 4' hydroxy or methoxy substituent blocks increased SIRT1 expression.
http://www.ncbi.nlm....pt=AbstractPlus
So do any other compounds fall into the blockage of activation of SIRT1 such as metabolites of quercetin or other compounds of interest?
This article is 41 pages LONG!