Yun-Hee Youm
Research & Publications
Biography
News
Research Summary
My research work is focused on studying the interactions between inflammation and metabolism, age-related thymic involution and degenerative disorders in the elderly, and centered on the understanding the role of hormones on the regulation of the immune system.
My studies unveil the molecular underpinnings of Immune-metabolic interactions at multiple aspects: 1) The NlRP3 inflammasome as an upstream target that control age-related inflammation and offer and innovative therapeutic strategy to lower NLRP3 activity to delay multiple age-related chronic diseases. - I have discovered that increased activation of NLRP3 inflammasome, a unique innate sensor in specialized cells called macrophages is responsible for the functional decline in the aging process (published in Cell Metabolism and Cell Reports). 2) Use of low carbohydrate or ketogenic diets could be relevant against several inflammatory disorders and pharmacological manipulation of BHB might be viable strategy for reducing inflammation. - I also discovered that a special diet that increases ketone bodies (our body’s alternate fuel that is derived from fat) can inhibit this inflammasome complex and alleviate inflammatory disease (published in Nature Medicine 2016). 3) I have been involved in the identifying the role of FGF21, a novel pro-longevity hormone in regulation of lifespan and healthspan. I have generated majority of the preliminary data and animal models in this project. - I also discovered that FGF21 a hormone that increases lifespan in mice can rejuvenate the immune system in the aged (published in PNAS 2016).
Selected Publications
- Obesity increases the production of pro-inflammatory mediators from adipose tissue T cells and compromises TCR repertoire diversity: Implications for systemic inflammation and insulin-resistance (87.32)Youm Y, Yang H, Badanmagsar B, Gimble J, Greenway F, Mynatt R. Obesity increases the production of pro-inflammatory mediators from adipose tissue T cells and compromises TCR repertoire diversity: Implications for systemic inflammation and insulin-resistance (87.32). The Journal Of Immunology 2010, 184: 87.32-87.32. DOI: 10.4049/jimmunol.184.supp.87.32.
- Proteomic analysis of androgen-independent growth in low and high passage human LNCaP prostatic adenocarcinoma cellsYoum YH, Kim S, Bahk YY, Yoo TK. Proteomic analysis of androgen-independent growth in low and high passage human LNCaP prostatic adenocarcinoma cells. BMB Reports 2008, 41: 722-727. PMID: 18959819, DOI: 10.5483/bmbrep.2008.41.10.722.
- Doxazosin-induced clusterin expression and apoptosis in prostate cancer cellsYoum YH, Yang H, Yoon YD, Kim DY, Lee C, Yoo TK. Doxazosin-induced clusterin expression and apoptosis in prostate cancer cells. Urologic Oncology Seminars And Original Investigations 2007, 25: 483-488. PMID: 18047956, DOI: 10.1016/j.urolonc.2007.02.010.
- MP-17.13: Silencing of clusterin gene with siRNA accelerates doxazosin induced apoptosis in PC-3 human prostate cancer cell linesCha G, Yoo T, Youm Y, Jo M, Lee C. MP-17.13: Silencing of clusterin gene with siRNA accelerates doxazosin induced apoptosis in PC-3 human prostate cancer cell lines. Urology 2007, 70: 133-134. DOI: 10.1016/j.urology.2007.06.500.
- MP-08.15 Prolonged culture of LNCaP prostate cancer cells leads to androgen independence and resistance to doxazosin induced apoptosis with clusterin up-regulationYoo T, Youm Y, Park H, Kang J, Park J, Kim T. MP-08.15 Prolonged culture of LNCaP prostate cancer cells leads to androgen independence and resistance to doxazosin induced apoptosis with clusterin up-regulation. Urology 2006, 68: 100-101. DOI: 10.1016/j.urology.2006.08.322.
- MP-21.19 The effects of URO-Dr® treatment and finasteride on the apoptosis of prostate in beagle dogsYoo T, Cho H, Youm Y, Park J, Kim T, Kim H. MP-21.19 The effects of URO-Dr® treatment and finasteride on the apoptosis of prostate in beagle dogs. Urology 2006, 68: 194. DOI: 10.1016/j.urology.2006.08.620.
- Apoptosis Induction and Clusterin Expression of NRP-152 Cells by TamsulosinYoum Y, Yoon Y, Woo J, Yoo T. Apoptosis Induction and Clusterin Expression of NRP-152 Cells by Tamsulosin. Journal Of The Korean Continence Society 2006, 10: 132. DOI: 10.5213/jkcs.2006.10.2.132.
- Less Keratinocyte-Derived Factors Related to More Keratinocyte Apoptosis in Depigmented than Normally Pigmented Suction-Blistered Epidermis May Cause Passive Melanocyte Death in VitiligoLee AY, Kim NH, Choi WI, Youm YH. Less Keratinocyte-Derived Factors Related to More Keratinocyte Apoptosis in Depigmented than Normally Pigmented Suction-Blistered Epidermis May Cause Passive Melanocyte Death in Vitiligo. Journal Of Investigative Dermatology 2005, 124: 976-983. PMID: 15854039, DOI: 10.1111/j.0022-202x.2005.23667.x.
- 407: Clusterin Expression and Apoptosis Induction by Doxazosin in Human Prostate Cancer CellsYoo T, Youm Y, Cho J, Kang J, Yang H, Kim D. 407: Clusterin Expression and Apoptosis Induction by Doxazosin in Human Prostate Cancer Cells. Journal Of Urology 2005, 173: 111. DOI: 10.1016/s0022-5347(18)34660-3.
- Keratinocytes in the depigmented epidermis of vitiligo are more vulnerable to trauma (suction) than keratinocytes in the normally pigmented epidermis, resulting in their apoptosisLee A, Youm Y, Kim N, Yang H, Choi W. Keratinocytes in the depigmented epidermis of vitiligo are more vulnerable to trauma (suction) than keratinocytes in the normally pigmented epidermis, resulting in their apoptosis. British Journal Of Dermatology 2004, 151: 995-1003. PMID: 15541077, DOI: 10.1111/j.1365-2133.2004.06136.x.