Psoriasis is a chronic autoimmune disease affecting millions worldwide, characterized by abnormal skin cell proliferation, inflammation, and immune dysregulation. Over the past few decades, significant advancements have been made in unraveling the intricate pathogenesis of psoriasis, shedding light on the underlying molecular mechanisms driving its development and progression. These advancements have paved the way for the development of targeted therapies, revolutionizing the management of this debilitating condition. Understanding the pathogenesis of psoriasis at a deeper level has provided valuable insights into potential therapeutic targets, offering new hope for more effective and personalized treatment approaches. These genetic variations impact various aspects of immune function, skin barrier integrity, and inflammatory responses, ultimately influencing an individual's predisposition to psoriasis. Furthermore, environmental factors play a significant role in triggering and exacerbating psoriasis symptoms. Smoking, obesity, alcohol consumption, and psychological stress have all been implicated as environmental triggers, exacerbating inflammation and disrupting immune homeostasis. These environmental influences can interact with genetic predispositions to modulate disease severity and treatment response. Moreover, epigenetic modifications, including DNA methylation, histone modifications, and non-coding RNA regulation, contribute to the dynamic regulation of gene expression in psoriasis.
HTML PDFShare this article
Journal of Dermatology and Dermatologic Diseases received 4 citations as per Google Scholar report
