Acne vulgaris is a chronic inflammatory human skin condition marked by seborrhoea, comedones, papules, nodules, pimples, and perhaps scarring on the face, neck, and back. The pathogenesis of acne is multifactorial. Traditionally, four distinct processes were believed to play critical roles: increased sebum production, alteration of keratinization processes leading to comedone formation, follicular colonization by Propionibacterium acnes (P. acnes). The main objective of this project is to highlight the emerging evidence in the complex pathogenesis of acne vulgaris and provide an overview of the novel molecules being evaluated for treatment of acne, with a short focus into relevant pathogenic pathways in relation to mechanisms of action of these novel therapeutic targets like PPAR modulators, anti-androgens, melanocortin receptor, IGF-1 inhibitors, Coenzyme-A Carboxylase Inhibitors, Retinoic acid receptor-γ agonist, Phosphodiesterase 4 inhibitor, Liver X-Receptor (LXR), NMDA antagonist, Stearoyl-CoA desaturase-1 inhibitor, Leukotriene A4 hydrolase inhibitor, Acetylcholine (Ach) inhibitors, Inhibitor of cathelicidin activation and metalloproteinases activity, Specific competitive inhibitor of 5α-reductase etc.
Gargi Pal1*, Dr. Pratap Chandra Pradhan2, Subhajit Makar3 (Wed,) studied this question.