Rodent models to evaluate the impact of cadmium exposure on atopic dermatitis.

Abstract

This review investigates the role of rodent models in elucidating the effects of cadmium exposure on atopic dermatitis (AD) pathology. Rodent models, particularly mice and rats, are instrumental in replicating the clinical, histological, and immunological characteristics of AD. These models offer critical insights into the disease's progression under environmental stressors like cadmium, emphasizing the interplay between genetic predisposition, immune dysregulation, and oxidative stress. Rodent models are categorized into spontaneous, genetically engineered, and induced types, each contributing uniquely to AD research. Spontaneous models naturally develop AD-like symptoms, while genetically engineered models, such as filaggrin-deficient mice, highlight the synergy between genetic predispositions and environmental triggers. Induced models, employing agents like oxazolone, simulate AD conditions exacerbated by cadmium exposure. This review addresses challenges such as dose selection, interspecies differences, and environmental factors affecting reproducibility and translation of rodent studies to human contexts. Recent advancements in OMICs technologies are explored, providing a comprehensive view of cadmium-induced molecular disruptions, including oxidative stress, immune dysregulation, and epigenetic modifications. A multidisciplinary approach combining toxicology, dermatology, and immunology insights underscores the potential for identifying novel therapeutic targets. These strategies aim to mitigate cadmium's harmful effects on AD and improve translational outcomes. Findings from this review demonstrate how rodent models enhance understanding of cadmium's impact on AD, offering significant potential for developing remediation strategies.