Recent publications highlight groundbreaking findings on the genetic mechanisms of heart disease, novel therapeutic approaches for heart failure, and innovative strategies for improving cardiovascular health outcomes.
In Mice Subjected to Chronic Stress, Exogenous cBIN1 Preserves Calcium-Handling Machinery and Cardiac Function
This study introduces the role of cBIN1-microdomains in organizing intracellular distribution of SERCA2a, which is disrupted in chronically stressed hearts with diastolic dysfunction. By normalizing cBIN1-microdomain via gene therapy, intracellular distribution of dyads and SERCA2a is reorganized to improve cardiac inotropy and lusitropy of failing hearts.
Liu Y, Zhou K, Li J, Agvanian S, Caldaruse AM, Shaw S, Hitzeman TC, Shaw RM, Hong T (2020).
JACC Basic Transl Sci, 5(6), 561-578.
The ESCRT-III pathway facilitates cardiomyocyte release of cBIN1-containing microparticles
This study introduces the mechanistic turnover of cardiomyocyte cBIN1-microdomains from normal and failing cardiomyocytes. cBIN1 interacts with an ESCRT-III member CHMP4B to release cBIN1-microparticles from cardiomyocyte membrane microdomains into circulation. The released cBIN1-microparticles carry cardiac specific signals serving as a marker of biochemical health of cardiomyocytes.
Xu B, Fu Y, Liu Y, Agvanian S, Wirka RC, Baum R, Zhou K, Shaw RM, Hong T (2017).
PLoS Biol, 15(8), e2002354.
Isoproterenol Promotes Rapid Ryanodine Receptor Movement to Bridging Integrator 1 (BIN1)-Organized Dyads
This study introduces the role of cBIN1-microdomains in organizing L-type calcium channel and ryanodine receptor couplons at dyads. The study also identifies the super dynamic feature of cBIN1-microdomains, which reorganize within 5 minutes of b-adrenergic activation for efficient excitation-contraction coupling during an acute stress response.
Fu Y, Shaw SA, Naami R, Vuong CL, Basheer WA, Guo X, Hong T (2016).
Circulation, 133(4), 388-97.