The study of the fungal communities of the skin constitutes a pivotal component of skin microbiome research. Within these communities, the genus Malassezia stands out as a major constituent, representing 50% to 80% of the total fungal colonization on the skin of healthy individuals. The excessive growth or metabolic irregularities of this genus are intimately connected with the onset of various skin disorders that are intrinsically linked to its lipid-dependent nature. Cutaneous lipid metabolism is indispensable for maintaining the skin barrier function and skin health. Malassezia possesses the ability to encode multiple lipase genes, and the secretion of these lipases plays a pivotal role in the survival strategies of the fungi. This review explores recent advances in the ecological niche of Malassezia in skin microecological homeostasis, its mechanism of disrupting skin lipids through catabolic metabolites, and the relationship between this disruption of the skin lipid barrier and skin diseases. This review offers a reference for future research on the mechanisms by which Malassezia affects lipid metabolism and provides a theoretical foundation for the development of innovative therapeutic approaches for dermatological conditions.

Squalane (SQ, a saturated, sebum-mimetic hydrocarbon), oleic acid (OA, a monounsaturated fatty acid), and linoleic acid (LA, a polyunsaturated essential fatty acid) belong to the category of “lipids and fats” in cosmetic materials, and are widely employed as skin-conditioning emollients. However, they present differences in UV stress. In this study, we compared their effects on UV-induced oxidative damage, inflammation, and lipid metabolism using a mouse model and human sebaceous gland cells (SZ95). Results showed that 10% SQ did not worsen oxidative damage or inflammation after 6 weeks of UV exposure. In contrast, the 5% and 10% OA/LA groups showed increased skin wrinkling (p < 0.01), epidermal thickening (p < 0.05), and sebaceous gland atrophy. Transcriptome analysis indicated OA/LA upregulated arachidonic acid-related cytokine pathways (PTGS2/IL-1β; p < 0.001). In SZ95 cells, 0.006% OA/LA significantly increased lipid droplet formation (p < 0.001), free fatty acid (FFA) levels (p < 0.001), and pro-inflammatory gene expression (p < 0.001). Conversely, SQ neither promoted lipid droplet/FFA secretion nor induced oxidative stress. These findings suggest that high concentrations of unsaturated fatty acids in skincare may worsen lipid dysregulation and inflammation, while formulations based on saturated hydrocarbons like SQ could provide superior photoaging management by stabilizing skin barrier function.

This review addresses the exposure risks associated with the inhalation of aerosolized cosmetic products and explores the utility of lung organoids in assessing these risks. Aerosolized cosmetics such as sprays pose potential health hazards through inhalation, necessitating a thorough evaluation of exposure levels. Traditional methods for assessing inhalation risks have limitations, prompting the exploration of more sophisticated models. Lung organoids, three-dimensional structures derived from stem cells, offer a biologically relevant model for studying lung responses to inhaled substances. This review discusses the construction of lung organoids, their characteristics, and the advantages that they provide over conventional models. Furthermore, it examines existing studies that have employed lung organoids to evaluate the effects of cosmetic inhalation exposure, highlighting the potential of this approach to enhance the safety assessments of cosmetic products. We aim to establish lung organoids as a reliable tool for future research, ensuring the safety and regulatory compliance of cosmetics.

Current acne therapies face major limitations, including antibiotic resistance and skin irritancy. In this study, a synergistic strategy combining cryptotanshinone and madecassoside was developed through functional complementarity. Antibacterial activity against Cutibacterium acnes was evaluated using minimum inhibitory concentration (MIC) and inhibition zone assays, while cytotoxicity was assessed using human keratinocytes (HaCaTs). Anti-inflammatory efficacy was quantified by measuring tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), interleukin-6 (IL-6), and prostaglandin E₂ (PGE₂) in lipopolysaccharide-stimulated macrophages and a copper sulfate (CuSO₄)-induced zebrafish inflammatory model. Systemic safety was examined in zebrafish models (developmental toxicity and sodium dodecyl sulfate-induced irritation). Finally, macroscopic severity, histopathology, and serum cytokines were used to assess an oleic acid-induced rat acne model. Cryptotanshinone inhibited Cutibacterium acnes (minimum inhibitory concentration = 62.5 μg/mL) but exhibited cytotoxicity (>5 μg/mL) and irritancy (≥1000 μg/mL). Madecassoside eliminated cryptotanshinone-induced cytotoxicity and reduced irritation. Importantly, the combination maintained antibacterial efficacy while synergistically enhancing anti-inflammatory effects, achieving a 94% reduction in follicular hyperkeratosis compared with 39% for cryptotanshinone alone (p < 0.01), alongside normalization of histopathology and cytokine levels. In conclusion, madecassoside functionally complements cryptotanshinone by neutralizing its cytotoxicity and irritancy, enabling a safe, synergistic therapy that concurrently targets antibacterial and anti-inflammatory pathways in acne pathogenesis