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Yuejin Wu, M.S., Ph.D.

Photo of Dr. Yuejin Wu, M.S., Ph.D.

Assistant Professor of Medicine


Yuejin Wu earned his Ph.D. in Pharmacology from Tongji Medical University in Wuhan, China in 1990. He has been trained at Peking University (China), University of Montreal (Canada), and Vanderbilt University (U.S.). Dr. Wu is a founding member of the Anderson lab and has contributed extensively to establishing electrophysiological studies, single cell isolation, and other functional experiments in the lab. He is currently focused on studies of the pacemaking mechanism of sinoatrial node cells, especially on the role of intracellular and mitochondrial calcium, as well as calmodulin kinase II regulation in pacemaking activity. more


  • Assistant Professor of Medicine

Departments / Divisions



  • M.S., Wuhan University (China) (1987)
  • Ph.D., Tongji Medical University (China) (1990)

Research & Publications


Research in the Anderson laboratory focuses on cellular signaling and ionic mechanisms that cause heart failure, arrhythmias and sudden cardiac death, major public health problems worldwide. Our primary focus is on the multifunctional Ca2+ and calmodulin-dependent protein kinase II (CaMKII). Our laboratory identified CaMKII as an important pro-arrhythmic and pro-cardiomyopathic signal. These studies have provided proof of concept evidence motivating active efforts in biotech and the pharmaceutical industry to develop therapeutic CaMKII inhibitory drugs to treat heart failure and arrhythmias.

CaMKII is activated by increased intracellular Ca2+ and oxidation. Diverse ‘upstream’ signals, including catecholamines and the renin-angiotensin-aldosterone pathway increase CaMKII activity. CaMKII is multifunctional because it has multiple ‘downstream’ targets. CaMKII catalyzed phosphorylation in myocardium appears to coordinate activity of many or most voltage-gated ion channels, Ca2+ homeostatic proteins and gene transcription events.

Under physiological conditions, CaMKII is important for excitation-contraction coupling and fight or flight increases in heart rate. However, myocardial CaMKII is excessively activated during disease conditions where it contributes to loss of intracellular Ca2+ homeostasis, membrane hyperexcitability, premature cell death, and hypertrophic and inflammatory transcription. These downstream targets appear to contribute coordinately and decisively to heart failure and arrhythmias. Recently, we have developed evidence that CaMKII also participates in asthma.

Lab Website: Anderson Lab

Selected Publications

Wu Y, Gao Z, Chen B, Koval OM, Singh MV, Guan X, Hund TJ, Kutschke WJ, Sarma S, Grumbach IM, Wehrens XHT, Mohler PJ, Song LS, Anderson ME. Calmodulin kinase II is required for fight or flight sinoatrial node physiology. Proc Natl Acad Sci U S A. 2009; 106(14):5972-7. Epub 2009 Mar 10.

Chen B, Wu Y, Mohler PJ, Anderson ME, Song LS. Local control of Ca2+-induced Ca2+ release in mouse sinoatrial node cells. J Mol Cell Cardiol. 2009; 47(5):706-15. Epub 2009 Jul 15.

Hall DD, Wu Y, Domann FE, Spitz DR, Anderson ME. Mitochondrial Calcium Uniporter Activity Is Dispensable for MDA-MB-231 Breast Carcinoma Cell Survival. PLoS One. 2014 May 6; 9(5):e96866. doi: 10.1371/journal.pone.0096866.

Wu Y, Anderson ME. CaMKII in sinoatrial node physiology and dysfunction. Front Pharmacol. 2014 Mar 18; 5:48. eCollection 2014.

Lai MH, Wu Y, Gao Z, Anderson ME, Dalziel JE, Meredith AL. BK channels regulate sinoatrial node firing rate and cardiac pacing in vivo. Am J Physiol Heart Circ Physiol. 2014 Nov 1;307(9):H1327-38. doi: 0.1152/ajpheart.00354.2014. Epub 2014 Aug 29. PubMed PMID: 25172903; PubMed Central PMCID: PMC4217012.

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