Andreas Koschinski

This study investigates the role of lysosomal Ca2+ signaling in heart rhythm and atrial function, finding that NAADP pathway inhibition affects SAN pacemaker activity and cAMP production in atrial myocytes.

This paper identifies a nanodomain mechanism regulating troponin I phosphorylation and demonstrates a peptide that selectively enhances relaxation without compromising systolic function in heart failure.

This study shows that lysosomal calcium signaling via NAADP and calcium-stimulated adenylyl cyclase 1 and 8 contributes to the acute α-adrenergic response in atrial myocytes.

This study shows that IP3R activation in atrial myocytes increases cAMP, which can be inhibited by IP3R blockers, but ventricular myocytes show cAMP increases independent of IP3R.