Juan C. Sáez is known for his studies on connexin-based gap junction and hemichannel functions under normal and pathological conditions. He provided the first evidence of connexin post translational modifications by phosphorylation and nitrosylation and gap junction permeability to IP3 and Ca2+. He has pioneered the view that immune system cells form transient gap junctions. He contributed to demonstrate that hemichannels can open in normal mammalian cells without affecting their viability but under pathological conditions are critical for the inflammasome activation in fast skeletal myofibers and glial cells of the brain. He also demonstrated the role of hemichannels in muscular dystrophies and several neurodegenerative diseases. He established a Chilean school of young investigators who are independently funded to study connexin and pannexin channels. He was born in Osorno-Chile (1956), obtained the degree of Biochemist, University of Concepcion, Chile (1979) and PhD in Sciences, Albert Einstein College of Medicine, Bronx, NY, USA (1986). He is Prof. of Physiology, Catholic University of Chile (1993-present) and of Neuroscience, University of Valparaíso (2018-present) and Deputy Director of the Interdisciplinary Neuroscience Center, University of Valparaíso (2010-present). He is member of the Latin American Academy of Science (2017) and National Academy of Science, USA.

Research Interests

Juan C. Sáez' laboratory is interested in advancing the knowledge on gating and regulatory mechanisms that control the open probability of hemichannels and gap junction channels formed by subunits of different protein families (connexins and pannexins in vertebrates and innexins in invertebrates). In addition, they search for new hemichannel blockers that could facilitate the demonstration of their functional roles in different pathophysiological conditions. Using bioinformatics tools, they discovered potent and selective connexin hemichannel blockers. These compounds have been useful to prevent muscle dysfunction associated to genetic muscular dystrophies such as Duchenne and Becker diseases. The latter demonstrates that inflammation triggered by the genetic condition and not the mutations themselves explain the tissue dysfunction. Currently, they are performing preclinical studies to validate the use of hemichannel blockers in clinical studies. Similarly, they found that acquired brain pathologies such as depression and epilepsy are associated to a significant increase in glial connexin hemichannel activity. They are currently testing whether neuroinflammation triggered early during specific stages of brain ontogeny leads to aberrant cellular migration and differentiation in distinct brain structures. The latter might provide an opportunity to prevent the development of psychiatric diseases not yet explained by mutations of specific genes.

Membership Type

International Member

Election Year


Primary Section

Section 23: Physiology and Pharmacology