R. John Solaro served as Head of the Department of Physiology and Biophysics at the University of Illinois Chicago (UIC) from 1988 to 2015. He moved to UIC from the University of Cincinnati College of Medicine. He trained for his PhD in the Department of Physiology at University of Pittsburgh School of Medicine and immediately moved on to a faculty position at the Medical College of Virginia. In 1975-76 he was a Fellow of the American and British Heart Associations and worked with S. V. Perry in Birmingham, England. He was an honorary research fellow in Physiology at Heidelberg University, Germany in 1979. In 1987 he was a Fogarty Fellow working with David Allen at University College London. Solaro was appointed Distinguished University Professor in the University of Illinois System in 1998. He is the founder and served as director of the UIC Center for Cardiovascular Research. At UIC, Solaro received the University Scholar Award, the Faculty of the Year Award, the Mentor of the Year Award, and the Distinguished Service Award. Solaro was a member of the NIH Physiology study section and is past Chair of the Skeletal Muscle and Exercise Physiology and the Cardiovascular Sciences study sections. He has served as Associate Editor and was elected as Editor-in-Chief of the Journal of Molecular and Cellular Cardiology beginning in 2017. He is past Associate Editor of the American Journal of Physiology (Heart). He has also served on the editorial boards of Circulation Research, the Journal of Clinical Investigation, and the Journal of Biological Chemistry.

Solaro is a world leader in the investigation of cardiac sarcomeres, the biological machine controlling the mechanical activity of the heart. Seminal and highly cited publications include the following: i) a method in world-wide use for the study of myofilament proteins using “detergent skinning” with Triton X-100; ii) three papers in Nature (2 in 1975 and one 1982) reported the first evidence that both cardiac troponin I ( TnI) and phospholamban could be phosphorylated in the beating heart inducing regulation of relaxation; iii) proof of principle that sarcomere proteins are targets for inotropic drugs now in clinical use; iv) studies emphasizing the role of sarcomeres not only as force and shortening machines, but as hubs of cell signaling; v) demonstration that slow skeletal TnI is the neonatal isoform and is cardio-protective; vi) demonstration that biased signaling via beta-arrestin at the AT1 receptor can control sarcomere response to Ca; vii) evidence that myofilament strain at the Z-disk provides a source of mechano-transduction; viii) evidence that use cTnI as a biomarker for MI is useful in patient stratification; ix) evidence that glutathionylation of cardiac MyBP-C3 is a potent regulator of cardiac dynamics and a potential biomarker for HFpEF; x) seminal evidence for a role of p21 activated kinase in cardiac regulation.

A dominant theme in the laboratory is integration of mechano-signaling and signal transduction at the level of cardiac sarcomeres to and from the walls of the chambers and to and from the micro-environment of the cardiac myocytes, including coronary endothelium, fibroblasts, and lymphocytes. Linkage of common cardiomyopathies to mutations in sarcomere proteins provided a strong underpinning for the further investigation of how a specific change at the level of the sarcomeres can induce adaptive and maladaptive cardiac remodeling and how therapeutic approaches may be developed.