Francisco J Alvarado, Pharm D, PhD

Research Interests

The long-term goal of the Alvarado Lab is to is to understand the mechanisms of heart disease and to develop safe and effective treatments that improve the life of patients. Our primary interest is the regulation of cardiac ion channels with emphasis on diseases arising from their dysfunction, especially calcium-dependent arrhythmias and structural cardiomyopathies. Calcium is required for heart function in a process called excitation-contraction coupling; yet, dysregulation of calcium homeostasis is known to participate in heart disease. We apply state-of-the art imaging, electrophysiology and cell biology tools to understand how mutations affecting proteins involved in excitation-contraction coupling, such the major intracellular calcium channel in the heart ryanodine receptor 2, participate in the development of disease and, therefore, can be targets for drug development.

Honor and awards

American Heart Association Career Development Award (2019)

School of Medicine and Public Health Centennial Scholar (2022)

Selected publications

Link to My Bibliography from PubMed: https://www.ncbi.nlm.nih.gov/myncbi/francisco.alvarado.1/bibliography/public/

1. Alvarado FJ, Chen X, Valdivia HH. Ablation of the cardiac ryanodine receptor phospho-site Ser2808 does not alter the adrenergic response or the progression to heart failure in mice. Elimination of the genetic background as critical variable. J Mol Cell Cardiol 2017;103:40-47.
2. Alvarado FJ, Bos JM, Yuchi Z, Valdivia CR, Hernández JJ, Zhao YT, Henderlong DS, Chen Y, Booher TR, Marcou CA, Van Petegem F, Ackerman MJ, Valdivia HH. Cardiac hypertrophy and arrhythmia in mice induced by a mutation in ryanodine receptor 2. JCI Insight 2019; 4:e126544.
3. Kim JC, Perez-Hernandez M, Alvarado FJ, Maurya SR, Montnach J, Tin Y, Zhang M, Lin X, Vasquez C, Heguy A, Liang F-X, Woo S-H, Morley GE, Rothenberg E, Lundby A, Valdivia HH, Cerrone M, Delmar M. Disruption of Ca2+i homeostasis and Cx43 hemichannel function in the right ventricle precedes overt arrhythmogenic cardiomyopathy in PKP2-deficient mice. Circulation 2019:140:1015-1030.
4. Reilly L, Alvarado FJ, Lang D, Abozeid S, Van Ert H, Spellman C, Warden J, Makielski JC, Glukhov AV and Eckhardt LL. Genetic Loss of IK1 Causes Adrenergic-Induced Phase 3 Early Afterdepolarizations and Polymorphic and Bidirectional Ventricular Tachycardia. Circ Arrhythm Electrophysiol. 2020;13:e008638.
5. Zheng J, Dooge HC, Perez-Hernandez M, Zhao YT, Chen X, Hernandez JJ, Valdivia CR, Palomeque J, Rothenberg E, Delmar M, Valdivia HH, Alvarado FJ. Preserved cardiac performance and adrenergic response in a rabbit model with decreased ryanodine receptor 2 expression. Journal of molecular and cellular cardiology. 2022;167:118-28.