Psoriasis: From Pathogenesis to Pharmacological and Nano-Technological-Based Therapeutics

Abstract

Research in the pathogenesis of inflammatory skin diseases, such as skin dermatitis and psoriasis, has experienced some relevant breakthroughs in recent years. The understanding of age-related factors, gender, and genetic predisposition of these multifactorial diseases has been instrumental for the development of new pharmacological and technological treatment approaches. In this review, we discuss the molecular mechanisms behind the pathological features of psoriasis, also addressing the currently available treatments and novel therapies that are under clinical trials. Innovative therapies developed over the last 10 years have been researched. In this area, advantages of nanotechnological approaches to provide an effective drug concentration in the disease site are highlighted, together with microneedles as innovative candidates for drug delivery systems in psoriasis and other inflammatory chronic skin diseases.

The Cytokine Mediated Molecular Pathophysiology of Psoriasis and Its Clinical Implications

“…Pustular psoriasis is the second most common type of psoriasis which presents clinically as sterile pustules [ 11 ]. It typically occurs in patients in their 40 s, although cases have been reported in infants and young children.…”

“…Both the innate and adaptive immune systems are responsible for psoriatic inflammation. Antimicrobial peptides (AMPs), such as LL-37, β-defensins, and S100 proteins, which are released secondary to keratinocyte stress (i.e., physical injury) can trigger and maintain the inflammatory pathway in psoriasis [ 11 ]. Particularly, LL-37 can complex with DNA and RNA to initiate psoriatic inflammation by stimulating plasmacytoid dendritic cells (pDCs) [ 11 ].…”

“…Antimicrobial peptides (AMPs), such as LL-37, β-defensins, and S100 proteins, which are released secondary to keratinocyte stress (i.e., physical injury) can trigger and maintain the inflammatory pathway in psoriasis [ 11 ]. Particularly, LL-37 can complex with DNA and RNA to initiate psoriatic inflammation by stimulating plasmacytoid dendritic cells (pDCs) [ 11 ]. The maintenance phase of psoriasis is primarily mediated by the adaptive immune system through the TNF-α/IL-23/IL-17 axis.…”

Analysis of PPARγ Signaling Activity in Psoriasis

“…Functions of IL17 and transcription factors we tested in this work are well studied in psoriasis (see more details in [22,26,27], and in our previous publications [28][29][30]). Other aspects of PPARγ related signalling pathways were also studied.…”

Lipid Nanocarriers for Hyperproliferative Skin Diseases

“…Psoriasis is a chronic inflammatory disease of the skin and joints, autoimmune, with great polymorphism of clinical expression [ 58 ]. This disease is one of the most frequently described dermatoses in clinical practice, affecting men and women in the same way, characterized by cell renewal seven times faster than for normal skin, which is 28 days [ 7 , 59 ].…”