Robert Barndt

1 Introduction Cardiac muscle contraction and relaxation are finely tuned by intracellular calcium homeostasis. During systole, membrane depolarization activates L-type calcium channels (LCCs), permitting calcium influx into the cytosol.

Abstract The R9C mutation of Phospholamban (PLN) leads to dilated cardiomyopathy (DCM) and premature death, yet its pathological role remains elusive in human cardiomyocytes. To address this knowledge gap, the current study generated PLN R9C knock-in (KI) and patient-specific induced pluripotent stem cell-derived cardiomyocytes (iPSC-CMs) for systematic examination of the expression profile, physiological function, and cellular signaling in mutation-carrying cells.

Investigating endogenous, cell stress, and acid-induced matriptase activation demonstrated those mechanisms were mediated ROS and could be inhibited by N-acetyl cysteine (NAC) It has been recently published that ROS and ERK were two pathways that mediated Etoposide-induced cytotoxicity in human kidney cell [33]. In Fig 3, we demonstrated that ERK (MAPK) inhibition did not induce matriptase activation, which suggested that Etoposide-induced matriptase activation could be ROS dependent.