Molecular Mechanisms of Thalidomide-induced Limb Malformations

Mebrie Zemene Kinde, Tewodoros Abere Mekuria

Abstract


Thalidomide is an immunomodulating and anticancer compound used in the treatment of malignancies, infectious and autoimmune diseases. In human medicine, exposure to thalidomide during pregnancy results in a wide range of anomalies mainly limb truncation, ear and eye malformation, with miscarriages or death in utero or soon after birth. Many animal models have been used in research to investigate the molecular mechanisms responsible for thalidomide teratogenic effect and showed similar development anomalies. As far as this, the exact mechanisms by which thalidomide induces developmental defects are not yet fully understood. However, several pathways including increased oxidative stress, impairing nuclear factor-kB activity, fibroblast growth factor 10 and fibroblast growth factor 8 downregulation, increased bone morphogen proteins expression and p53 activity, and inhibiting angiogenesis have been widely proposed. In general, it looks like that thalidomide embryopathy is a multifactorial event and further studies are needed to clarify the possible interactions involving different pathways. This paper is a short review of the current literature about the molecular mechanisms of thalidomide-induced limb malformations and their effects on the embryonic development.


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ISSN : 2251-1563