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2017 ; 15
(1
): 195
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p53: key conductor of all anti-acne therapies
#MMPMID28927457
Melnik BC
J Transl Med
2017[Sep]; 15
(1
): 195
PMID28927457
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This review based on translational research predicts that the transcription
factor p53 is the key effector of all anti-acne therapies. All-trans retinoic
acid (ATRA) and isotretinoin (13-cis retinoic acid) enhance p53 expression.
Tetracyclines and macrolides via inhibiting p450 enzymes attenuate ATRA
degradation, thereby increase p53. Benzoyl peroxide and hydrogen peroxide elicit
oxidative stress, which upregulates p53. Azelaic acid leads to mitochondrial
damage associated with increased release of reactive oxygen species inducing p53.
p53 inhibits the expression of androgen receptor and IGF-1 receptor, and induces
the expression of IGF binding protein 3. p53 induces FoxO1, FoxO3, p21 and
sestrin 1, sestrin 2, and tumour necrosis factor-related apoptosis-inducing
ligand (TRAIL), the key inducer of isotretinoin-mediated sebocyte apoptosis
explaining isotretinoin's sebum-suppressive effect. Anti-androgens attenuate the
expression of miRNA-125b, a key negative regulator of p53. It can thus be
concluded that all anti-acne therapies have a common mode of action, i.e.,
upregulation of the guardian of the genome p53. Immortalized p53-inactivated
sebocyte cultures are unfortunate models for studying acne pathogenesis and
treatment.
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