Dysregulation of the actin cytoskeleton in glomerular podocytes plays a key part in the development of proteinuria associated with chronic kidney diseases (CKDs). The GTPase dynamin — which is essential for podocyte structure and function — has been shown to undergo actin-dependent oligomerization, to regulate the actin cytoskeleton of the cell. Here, Schiffer et al. report that the small molecule Bis-T-23 promotes dynamin oligomerization in zebrafish and mice, to restore podocyte function and attenuate transient proteinuria. Moreover, Bis-T-23 reversed proteinuria in diverse mouse models of CKD, significantly extending lifespan.
References
Schiffer, M. et al. Pharmacological targeting of actin-dependent dynamin oligomerization ameliorates chronic kidney disease in diverse animal models. Nat. Med. http://dx.doi.org/10.1038/nm.3843 (2015)
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Crunkhorn, S. Targeting dynamin oligomerization. Nat Rev Drug Discov 14, 460 (2015). https://doi.org/10.1038/nrd4676
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DOI: https://doi.org/10.1038/nrd4676
