This hypothesis presents acne as a PI3K-Akt-mTORC1-driven pro-survival disease of the sebaceous follicle with impaired TRAIL-mediated death signalling. It is predicted that anti-acne agents such as isotretinoin enhance death signalling and thereby readjust the disturbed balance of pro-survival and death signalling of the sebaceous follicle in acne vulgaris. For this purpose, immortalized sebocyte cultures are regarded as inapproproate models to study the key features of acne pathogenesis.
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Bodo C. Melnik (2016) studied this question.
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