Melnik, Bodo C. and Schmitz, Gerd (2013) Are therapeutic effects of antiacne agents mediated by activation of FoxO1 and inhibition of mTORC1? EXPERIMENTAL DERMATOLOGY, 22 (7). pp. 502-504. ISSN 0906-6705, 1600-0625
Full text not available from this repository. (Request a copy)Abstract
Acne pathogenesis has recently been linked to decreased nuclear FoxO1 levels and increased mTORC1 activity. This hypothesis postulates that antiacne agents either enhance nuclear FoxO activity or inhibit mTORC1. Benzoyl peroxide (BPO), by activation of oxidative stress-inducible kinases, increases nuclear FoxO levels promoting Sestrin3-mediated AMPK activation. Furthermore, BPO-derived ROS may activate AMPK via ataxia-telangiectasia mutated. Isotretinoin and all-trans retinoic acid may stimulate FoxO gene expression. Doxycycline may enhance FoxOs nuclear retention by inhibiting the expression of exportin 1. Suppression of TNF signalling by tetracyclines, erythromycin and other macrolides may attenuate IKK-TSC1-mediated mTORC1 activation. Erythromycin attenuates ERK1/2 activity and thereby increases TSC2. Azelaic acid may decrease mTORC1 by inhibiting mitochondrial respiration, increasing cellular ROS and nuclear FoxO levels. Antiandrogens may attenuate mTORC1 by suppressing mTORC2-mediated Akt/TSC2 signalling. This hypothesis unmasks a common mode of action of antiacne agents as either FoxO enhancers or mTORC1 inhibitors and thus provides a rational approach for the development of new antiacne agents.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | TRANSCRIPTION FACTORS; OXIDATIVE STRESS; BENZOYL PEROXIDE; HUMAN SEBOCYTES; RETINOIC ACID; ACNE; EXPRESSION; APOPTOSIS; CANCER; AKT; acne; antiacne drugs; FoxOs; mTORC1; mTORC1 inhibitors |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Klinische Chemie und Laboratoriumsmedizin |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 07 Apr 2020 09:14 |
| Last Modified: | 07 Apr 2020 09:14 |
| URI: | https://pred.uni-regensburg.de/id/eprint/16465 |
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