PhytoSERM (phyto = plant, SERM = selective estrogen receptor modulator) is the medical term used to describe botanically derived substances that have been scientificaly proven to possess SERM qualities[1], similar to synthetically manufactured drugs of the same category.
[edit] Mechanism of action
Similarly to SERMs, phyto-SERMs act on the estrogen receptor in a selective manner, either as agonists, or as antagonists, thereby granting the possibility to selectively stimulate or inhibit estrogen-like responses in different tissues. The molecular basis for this discrimination lies in the variability of transcription coregulators in different tissues which interact with the estrogen receptor.[2] Furthermore many phytoestrogen (including phyto-SERMs) appear to be somewhat selective in binding for the estrogen receptor beta (ERβ) compared to the estrogen receptor alpha (ERα) paralog.[3][4] These two forms of the estrogen receptor display somewhat different tissue distributions[5] and regulate a partially-overlapping set of genes.[6][7]
PhytoSERMs' unique mechanism of action, being able to target specific tissues precisely while unaffecting others, may make them safer candidates for treatment of estrogen deficiencies.
[edit] Category members
[edit] Indications
PhytoSERMs are suitable for treating estrogen deficiencies that cause menopause symptoms, osteopenia and osteoporosis.
[edit] References
- ^ Boudes P, Bailly G (2000). "[Endocrinolgy of estrogens: some recent developments and future applications]" (in French). Therapie 55 (2): 237–47. PMID 10967695.
- ^ Dutertre M, Smith CL (November 2000). "Molecular mechanisms of selective estrogen receptor modulator (SERM) action". J. Pharmacol. Exp. Ther. 295 (2): 431–7. PMID 11046073. http://jpet.aspetjournals.org/cgi/content/abstract/295/2/431.
- ^ An J, Tzagarakis-Foster C, Scharschmidt TC, Lomri N, Leitman DC (May 2001). "Estrogen receptor beta-selective transcriptional activity and recruitment of coregulators by phytoestrogens". J. Biol. Chem. 276 (21): 17808–14. doi:10.1074/jbc.M100953200. PMID 11279159.
- ^ Chang EC, Charn TH, Park SH, Helferich WG, Komm B, Katzenellenbogen JA, Katzenellenbogen BS (May 2008). "Estrogen Receptors alpha and beta as determinants of gene expression: influence of ligand, dose, and chromatin binding". Mol. Endocrinol. 22 (5): 1032–43. doi:10.1210/me.2007-0356. PMID 18258689.
- ^ Couse JF, Lindzey J, Grandien K, Gustafsson JA, Korach KS (November 1997). "Tissue distribution and quantitative analysis of estrogen receptor-alpha (ERalpha) and estrogen receptor-beta (ERbeta) messenger ribonucleic acid in the wild-type and ERalpha-knockout mouse". Endocrinology 138 (11): 4613–21. doi:10.1210/en.138.11.4613. PMID 9348186.
- ^ Hurst AG, Goad DW, Mohan M, Malayer JR (October 2004). "Independent downstream gene expression profiles in the presence of estrogen receptor alpha or beta". Biol. Reprod. 71 (4): 1252–61. doi:10.1095/biolreprod.104.029421. PMID 15201200.
- ^ Kian Tee M, Rogatsky I, Tzagarakis-Foster C, Cvoro A, An J, Christy RJ, Yamamoto KR, Leitman DC (March 2004). "Estradiol and selective estrogen receptor modulators differentially regulate target genes with estrogen receptors alpha and beta". Mol. Biol. Cell 15 (3): 1262–72. doi:10.1091/mbc.E03-06-0360. PMID 14699072.
- ^ Somjen D, Katzburg S, Knoll E, et al. (May 2007). "DT56a (Femarelle): a natural selective estrogen receptor modulator (SERM)". J. Steroid Biochem. Mol. Biol. 104 (3-5): 252–8. doi:10.1016/j.jsbmb.2007.03.004. PMID 17428655.
[edit] See also
