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. 2018 Apr 5;9(1):246–257. doi: 10.1080/19491034.2018.1460045

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© 2018 The Author(s). Published by Informa UK Limited, trading as Taylor & Francis Group

This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License ( http://creativecommons.org/licenses/by-nc/4.0/), which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 1. — Specificity of a wide spectrum of treatment strategies for progeria. Several therapeutic strategies for progeria are shown. In decreasing order for their target specificity, treatment strategies can be mentioned as follows: the mutation-causing disease repair by genome editing (CRISPR as a future possibility to be evaluated), the inhibition of pre-mRNA aberrant splicing (Antisense OligoNucleotides: AONs, Metformin, MG132), the reduction of isoprenylated and methylated progerin levels (Farnesyl transferase inhibitors: FTIs, ZOledronate-PRAvastatin: ZOPRA, Monoaminopyrimidines: Mono-APs, Isoprenylcysteine CarboxyMethyl Transferase (ICMT) inhibitor, GeranylGeranylTransferase Inhibitor: GGTI-2147), the induction of progerin clearance (Rapamycin, Sulforaphane, Retinoids, MG132) and the reduction of the noxious downstream effects due to progerin accumulation (Rock inhibitor: Y-27632, Nuclear factor erythroid-2-Related Factor 2: NRF2 reactivation, Methylene blue, sodium salicylate, DOT1L inhibitor: epz-4777, Remodelin, Vitamin D, Resveratrol, N-Acetyl-Cysteine: NAC, inorganic pyrophosphate: PPi and JH4).