J
Jun-Ki Min
Researcher at Catholic University of Korea
Publications - 113
Citations - 3514
Jun-Ki Min is an academic researcher from Catholic University of Korea. The author has contributed to research in topics: Arthritis & T cell. The author has an hindex of 36, co-authored 111 publications receiving 3079 citations. Previous affiliations of Jun-Ki Min include The Catholic University of America.
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Grape seed proanthocyanidin extract (GSPE) differentially regulates Foxp3(+) regulatory and IL-17(+) pathogenic T cell in autoimmune arthritis.
Mi-Kyung Park,Jin-Sil Park,Mi-La Cho,Hye-Jwa Oh,Yu-Jung Heo,Yun-Ju Woo,Yang-Mi Heo,Min-Jung Park,H.J. Park,Sung-Hwan Park,Ho-Youn Kim,Jun-Ki Min +11 more
TL;DR: The results suggest that GSPE possesses a reciprocal control over IL-17 and Foxp3, which may serve as a possible novel therapeutic agent for inflammatory and autoimmune diseases, including rheumatoid arthritis.
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Toll-like receptor 2 and 4 combination engagement upregulate IL-15 synergistically in human rheumatoid synovial fibroblasts.
Young Ok Jung,Mi-La Cho,Chang-Min Kang,Joo-Yeon Jhun,Jin-Sil Park,Hye-Joa Oh,Jun-Ki Min,Sung-Hwan Park,Ho-Youn Kim +8 more
TL;DR: TLR2 activation in RA FLS by microbial constituents is involved in the induction of IL-15 and that TLR2 promotes inflammation through NF-kappaB is suggested, possibly contributing to the maintenance of synovitis in patients with RA.
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Temporal differential effects of proinflammatory cytokines on osteoclastogenesis
Su-Jin Moon,Inhye E. Ahn,Hyerin Jung,Hyoju Yi,Juryun Kim,Youngkyun Kim,Seung Ki Kwok,Kyung-Su Park,Jun-Ki Min,Sung-Hwan Park,Ho-Youn Kim,Ji Hyeon Ju +11 more
TL;DR: Targeting IL-1β may be a promising strategy to inhibit inflammation-associated bone destruction and osteoporosis according to the phase of osteoclast maturation.
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Eupatilin Exerts Antinociceptive and Chondroprotective Properties in a Rat Model of Osteoarthritis by Downregulating Oxidative Damage and Catabolic Activity in Chondrocytes.
TL;DR: It is suggested that eupatilin suppresses oxidative damage and reciprocally enhances extracellular matrix production in articular chondrocytes, making eup atilin a promising therapeutic option for the treatment of OA.
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IL-23 induces receptor activator of NF-kappaB ligand expression in fibroblast-like synoviocytes via STAT3 and NF-kappaB signal pathways.
Xia Li,Kyoung-Woon Kim,Mi-La Cho,Ji Hyeon Ju,Chang-Min Kang,Hye-Joa Oh,Jun-Ki Min,Sang Heon Lee,Sung-Hwan Park,Ho-Youn Kim +9 more
TL;DR: Interleukin appears to induce joint inflammation and bone destruction by stimulating RANKL expression in RA-FLS, and interactions between IL-23 and FLS indicate possible new therapeutic approaches for treating bone destruction in patients with inflammatory diseases.