{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T17:09:04Z","timestamp":1792516144456,"version":"4.5.0"},"reference-count":14,"publisher":"MDPI AG","issue":"6","license":[{"start":{"date-parts":[[2021,3,15]],"date-time":"2021-03-15T00:00:00Z","timestamp":1615766400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["IJMS"],"abstract":"<jats:p>Psoriasis is a chronic inflammatory skin disease characterized by IL-17-dominant abnormal innate and acquired immunity, and the hyperproliferation and aberrant differentiation of epidermal keratinocytes, and comorbid arthritis or cardiometabolic diseases. This Special Issue presented updated information on pathogenesis, comorbidities, and therapy of psoriasis. The pathogenesis of psoriasis may involve the dysfunction of indoleamine 2,3-dioxygenase 2 or of UBA domain containing 1-mediated regulation of CARD14\/CARMA2sh. The blood cells of psoriasis patients showed the enhanced oxidative stress\/autophagy flux and decreased 20S proteasome activity. Elafin, clusterin, or selenoprotein P may act as biomarkers for psoriasis and comorbid metabolic diseases. The proteomic profile of psoriasis lesions showed the dysfunction of dermal fibroblasts; up-regulation of proinflammatory factors and signal transduction or down-regulation of structural molecules. The skin inflammation in psoriasis may populate certain gut bacteria, such as Staphylococcus aureus and Streptococcus danieliae, which worsen the skin inflammation in turn. The psoriasis-associated pruritus may be caused by immune, nervous, or vascular mechanisms. In addition to current oral treatments and biologics, a new treatment option for psoriasis is now being developed, such as retinoic-acid-receptor-related orphan nuclear receptor \u03b3t inhibitors, IL-36 receptor antagonist, or aryl hydrocarbon receptor agonist. Antimicrobial peptides and innate immune cells, involved in the pathogenesis of psoriasis, may be novel therapeutic targets. The pathomechanisms and responses to drugs in collagen diseases are partially shared with and partially different from those in psoriasis. Certain nutrients can exacerbate or regulate the progress of psoriasis. The articles in this Special Issue will encourage attractive approaches to psoriasis by future researchers.<\/jats:p>","DOI":"10.3390\/ijms22062979","type":"journal-article","created":{"date-parts":[[2021,3,15]],"date-time":"2021-03-15T11:38:58Z","timestamp":1615808338000},"page":"2979","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":74,"title":["Psoriasis: Pathogenesis, Comorbidities, and Therapy Updated"],"prefix":"10.3390","volume":"22","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-4389-2312","authenticated-orcid":false,"given":"Naoko","family":"Kanda","sequence":"first","affiliation":[{"name":"Department of Dermatology, Nippon Medical School Chiba Hokusoh Hospital, Inzai, Chiba 2701694, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1968","published-online":{"date-parts":[[2021,3,15]]},"reference":[{"key":"ref_1","doi-asserted-by":"crossref","unstructured":"Mazzone, P., Congestr\u00ec, M., Scudiero, I., Polvere, I., Voccola, S., Zerillo, L., Telesio, G., Vito, P., Stilo, R., and Zotti, T. (2020). UBAC1\/KPC2 Regulates TLR3 Signaling in Human Keratinocytes through Functional Interaction with the CARD14\/CARMA2sh-TANK Complex. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21249365"},{"key":"ref_2","doi-asserted-by":"crossref","unstructured":"Karabowicz, P., Wro\u0144ski, A., Ostrowska, H., Waeg, G., Zarkovic, N., and Skrzydlewska, E. (2020). Reduced Proteasome Activity and Enhanced Autophagy in Blood Cells of Psoriatic Patients. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21207608"},{"key":"ref_3","doi-asserted-by":"crossref","unstructured":"Holmannova, D., Borsky, P., Borska, L., Andrys, C., Hamakova, K., Rehacek, V., Svadlakova, T., Malkova, A., Beranek, M., and Palicka, V. (2020). Metabolic Syndrome, Clusterin and Elafin in Patients with Psoriasis Vulgaris. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21165617"},{"key":"ref_4","doi-asserted-by":"crossref","unstructured":"Fujii, K., Yamamoto, Y., Mizutani, Y., Saito, K., and Seishima, M. (2020). 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The Role of Gut Microbiome in Psoriasis: Oral Administration of Staphylococcus aureus and Streptococcus danieliae Exacerbates Skin Inflammation of Imiquimod-Induced Psoriasis-Like Dermatitis. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21093303"},{"key":"ref_8","doi-asserted-by":"crossref","unstructured":"Komiya, E., Tominaga, M., Kamata, Y., Suga, Y., and Takamori, K. (2020). Molecular and Cellular Mechanisms of Itch in Psoriasis. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21218406"},{"key":"ref_9","doi-asserted-by":"crossref","unstructured":"Tokuyama, M., and Mabuchi, T. (2020). New Treatment Addressing the Pathogenesis of Psoriasis. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21207488"},{"key":"ref_10","doi-asserted-by":"crossref","unstructured":"Takahashi, T., and Yamasaki, K. (2020). Psoriasis and Antimicrobial Peptides. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21186791"},{"key":"ref_11","doi-asserted-by":"crossref","unstructured":"Sato, Y., Ogawa, E., and Okuyama, R. (2020). Role of Innate Immune Cells in Psoriasis. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21186604"},{"key":"ref_12","doi-asserted-by":"crossref","unstructured":"Ple\u0144kowska, J., Gabig-Cimi\u0144ska, M., and Mozolewski, P. (2020). Oxidative Stress as an Important Contributor to the Pathogenesis of Psoriasis. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21176206"},{"key":"ref_13","doi-asserted-by":"crossref","unstructured":"Yamamoto, T. (2020). Psoriasis and Connective Tissue Diseases. Int. J. Mol. Sci., 21.","DOI":"10.3390\/ijms21165803"},{"key":"ref_14","doi-asserted-by":"crossref","unstructured":"Kanda, N., Hoashi, T., and Saeki, H. (2020). Nutrition and Psoriasis. Int. J. Mol. 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