pubmed-article:21519409 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:21519409 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:21519409 | lifeskim:mentions | umls-concept:C0702166 | lld:lifeskim |
pubmed-article:21519409 | lifeskim:mentions | umls-concept:C0036505 | lld:lifeskim |
pubmed-article:21519409 | lifeskim:mentions | umls-concept:C0699748 | lld:lifeskim |
pubmed-article:21519409 | lifeskim:mentions | umls-concept:C1519814 | lld:lifeskim |
pubmed-article:21519409 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:21519409 | pubmed:dateCreated | 2011-4-26 | lld:pubmed |
pubmed-article:21519409 | pubmed:abstractText | The pathogenesis of acne, a disease of the pilosebaceous follicle and one of the most common chronic skin disorders, is attributed to multiple factors such as increased sebum production, alteration of the quality of sebum lipids, inflammatory processes, dysregulation of the hormone microenvironment, interaction with neuropeptides, follicular hyperkeratinisation and the proliferation of Propionibacterium acnes within the follicle. In particular, the sebaceous gland plays an exquisite role in the initiation of the disease as it possesses all the enzyme machinery for the production of hormones and cytokines. In addition, in response to the altered tissue environment in the pilosebaceous follicle as well as in answer to emotional fret, stress response system mechanisms with induction of central and local expression of neuropeptides, are also initiated. This review summarises the latest advances in understanding the role of sebaceous gland cells in the pathomechanism of acne. | lld:pubmed |
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