Ming Xu, Ph.D.Assistant Professor, UConn Center on Aging and the Department of Genetics & Genome Sciences
|B.S.||Fudan University||Biological Science|
|Ph.D.||University of Kansas Medical Center (KUMC)||Rehabilitation Science|
|Graduate Research Assistant||University of Kansas Medical Center||Graduate Research Assistant, Department of Physical Therapy and Rehabilitation Science, Dr. Hao Zhu’s Lab|
|Fellowship||Mayo Clinic||Research Fellow, Department of Internal Medicine, Dr. James L. Kirkland’s Lab|
|Research Associate||Mayo Clinic||Research Associate, Department of Internal Medicine, Dr. James L. Kirkland’s Lab|
|Name of Award/Honor||Awarding Organization|
|Postdoctoral Transition Awards in Aging||The Irene Diamond Fund/AFAR|
|Career Development Award||Regenerative Medicine Initiative for Diabetes|
|Postdoctoral Fellowship Program for Translational Research on Aging||Glenn/AFAR|
|Travel award, 2013 Alliance for Healthy Aging Symposium Held in the University Medical Center, Groningen, Netherlands||Alliance for Healthy Aging Symposium|
|Student Union Corporation Travel Scholarship||KUMC|
|Dean’s Diversity Scholarship, School of Allied Health||KUMC|
|School of Allied Health Scholarship Award||KUMC|
|First Place Award of Molecular and Cell Biology Session III Student Research Forum||KUMC|
|Third Place Award, National Mathematics Contest (High School), China|
|Name & Description||Category||Role||Type||Scope||Start Year||End Year|
|Ad hoc Reviewer for Scientific Journals (2012 - Present): Diabetes, Cell Metabolism, Aging Cell, FASEBJ, Trends in Endocrinology and Metabolism, Journal of Gerontology, Molecular and Cellular Biochemistry, Hormone and Metabolic Research||Professional/Scientific Journal||Ad hoc Reviewer||External||National||2012|
Aging is the biggest risk factor for most of the chronic diseases. The key goal for my lab is to discover novel interventions to slow down the aging process, and thereby alleviate a number of diseases simultaneously (https://today.uconn.edu/school-stories/new-uconn-health-aging-researcher-mission-promote-healthy-aging/). My recent work has demonstrated the efficacy of several drugs in extending the lifespan, maintaining physical function, and alleviating a range of diseases in aged mice, indicating the feasibility of this strategy.
Cellular senescence is one of the major players contributing to the fundamental aging process. My lab is leveraging novel mouse models and primary human cells as tools to examine the role and underlying mechanism of senescent cells in various conditions in mammals, and we aim to find new drugs to target senescent cells in order to alleviate a range of diseases as a group.
We have 3 major research directions.
1. To investigate the role of senescent cells in diseases. We are especially interested in diabetes, Alzheimer's disease, frailty, bone-related diseases, bladder dysfunction, and flu infection. We will be using novel transgenic mice and transplantation models for this.
2. To reveal the heterogeneity and transcriptomic signatures of senescent cells in vivo. We will be using single cell transcriptome technology to look at the senescent cells at different tissues under different biological conditions (aging, obesity or injury).
3. To screen for novel compounds to kill senescent cells. We are in the process of screening several libraries of compounds on human senescent cells, and expect to find a number of novel candidates. We will then further test these compounds in aged mice and human tissues.
|Title or Abstract||Type||Sponsor/Event||Date/Year||Location|
|Senescence and Senolytics||Panel Discussion||U13 Bench-to-Bedside Conference Series Osteoporosis and Soft Tissue||2019||Bethesda, MD|
|Blocking the senescence-associated secretory phenotype (SASP) reduces osteoclastogenesis and prevents age-related bone loss||Poster||American Society for Bone and Mineral Research 2015 Annual Meeting||2015||Seattle|
|The role of cellular senescence in age-related tissue dysfunction and diseases||Poster||Paul F. Glenn/AFAR Conf on Biology of Aging 28th Annual AFAR Grantee Conf.||2015||Santa Barbara|
|The bystander and systematic adverse effects of senescent preadipocytes||Poster||Experimental Biology 2014||2014||San Diego|
|Local and systematic adverse effects of senescent preadipocytes||Poster||Gerontological Society of America Annual Scientific Meeting 2013||2013||New Orleans|
|Local and systematic adverse effects of senescent preadipocytes||Poster||Alliance for Healthy Aging Symposium||2013||University Medical Center, Groningen, Netherlands|
|Local and systematic adverse effects of senescent preadipocytes||Poster||Gordon Research Conference (GRC) on Biology of Aging||2013||Lucca (Barga), Italy|
|Senescent cells compromise fat tissue functions||Poster||3rd Ann. Robert & Arlene Kogod Ctr on Aging Conf: Senescence & Healthspan||2012||Mayo clinic|
|Senescent cells compromise fat tissue functions||Panel Discussion||Intern. Federation for Adipose Therapeutics and Science, 10th Ann. Meeting||2012||Québec City, Canada|
|Ncb5or deficiency increases fatty acid catabolism and oxidative stress||Poster||2011 Liver Symposium, The Liver Center, Univ. of Kansas Medical Center||2011||Kansas City, Kansas|
|Ncb5or deficiency increases fatty acid catabolism and oxidative stress||Poster||Ann. Mtg of American Soc. for Biochem. and Molecular Biology (Exp. Biol.)||2011||Washington, D.C.|
|Ncb5or deficiency increases fatty acid catabolism and oxidative stress||Panel Discussion||Student Research Forum, Univ. of Kansas Medical Center||2011||Kansas City, Kansas|
|Defect in fatty acid desaturation leads to lipoatrophy through mitochondrial over-proliferation and compensation from de novo synthesis in Ncb5or null mice||Talk||Student Research Forum, Univ. of Kansas Medical Center||2009||Kansas City, Kansas|
|Fatty acid metabolism, diabetes and lipoatrophy in Ncb5or knockout mice||Poster||Student Research Forum, Univ. of Kansas Medical Center||2008||Kansas City, Kansas|