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

ABSTRACT: 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 differed from acute cardiac Mcu deletion in response to adrenergic stimulation and ischemia/reperfusion (I/R) injury, despite equivalent inactivation of rapid mitochondrial Ca²⁺ uptake. To explore this discrepancy between chronic and acute loss of uniporter activity, we compared short-term and long-term Emre de

SUBMITTER: Chapoy Villanueva H 

PROVIDER: S-EPMC10524693 | biostudies-literature | 2023 Aug

REPOSITORIES: biostudies-literature