Distinct effects of cardiac mitochondrial calcium uniporter inactivation via EMRE deletion in the short and long term

Transport of Ca2+ into mitochondria is thought to stimulate the production of ATP, a critical process in the heart's fight or flight response, but excess Ca2+ can trigger cell death. The mitochondrial Ca2+ uniporter complex is the primary route of Ca2+ transport into mitochondria, in which the channel-forming protein MCU and the regulatory protein EMRE are essential for activity. In previous studies, chronic Mcu or Emre deletion differ from acute cardiac Mcu deletion in response to adrenergic stimulation and ischemia/reperfusion (I/R) injury, despite equivalent inactivation of rapid mitochondrial Ca2+ uptake.

Source: Journal of Molecular and Cellular Cardiology - May 23, 2023 Category: Cytology Authors: Hector Chapoy Villanueva, Jae Hwi Sung, Jackie A. Stevens, Michael J. Zhang, Peyton M. Nelson, Saahiti Denduluri, Feng Feng, Timothy D. O'Connell, DeWayne Townsend, Julia C. Liu Source Type: research