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Nutritional Sensor REDD1 in Cancer and Inflammation: Friend or Foe?статья
Статья опубликована в высокорейтинговом журнале
Статья опубликована в журнале из списка Web of Science и/или Scopus- Авторы: Zhidkova Ekaterina M., Lylova Evgeniya S., Grigoreva Diana D., Kirsanov Kirill I., Osipova Alena V., Kulikov Evgeny P., Mertsalov Sergey A., Belitsky Gennady A., Budunova Irina, Yakubovskaya Marianna G., Lesovaya Ekaterina A.
- Журнал: International Journal of Molecular Sciences
- Том: 23
- Номер: 17
- Год издания: 2022
- Издательство: MDPI
- Местоположение издательства: Basel, Switzerland
- Первая страница: 9686
- Последняя страница: 9699
- DOI: 10.3390/ijms23179686
- Аннотация: Regulated in Development andDNADamage Response 1 (REDD1)/DNA Damage-Induced Transcript 4 (DDIT4) is an immediate early response gene activated by different stress conditions, including growth factor depletion, hypoxia, DNA damage, and stress hormones, i.e., glucocorticoids. The most known functions of REDD1 are the inhibition of proliferative signaling and the regulation of metabolism via the repression of the central regulator of these processes, the mammalian target of rapamycin (mTOR). The involvement of REDD1 in cell growth, apoptosis, metabolism, and oxidative stress implies its role in various pathological conditions, including cancer and inflammatory diseases. Recently, REDD1 was identified as one of the central genes mechanistically involved in undesirable atrophic effects induced by chronic topical and systemic glucocorticoids widely used for the treatment of blood cancer and inflammatory diseases. In this review, we discuss the role of REDD1 in the regulation of cell signaling and processes in normal and cancer cells, its involvement in the pathogenesis of different diseases, and the approach to safer glucocorticoid receptor (GR)- targeted therapies via a combination of glucocorticoids and REDD1 inhibitors to decrease the adverse atrophogenic effects of these steroids.
- Добавил в систему: Жидкова Екатерина Михайловна