Mitochondrial membrane potential instability on reperfusion after ischemia does not depend on mitochondrial Ca²⁺ uptake.

ABSTRACT: Physiologic Ca²⁺ entry via the Mitochondrial Calcium Uniporter (MCU) participates in energetic adaption to workload but may also contribute to cell death during ischemia/reperfusion (I/R) injury. The MCU has been identified as the primary mode of Ca²⁺ import into mitochondria. Several groups have tested the hypothesis that Ca²⁺ import via MCU is detrimental during I/R injury using genetically-engineered mouse models, yet the results from these studies are inconclusive. Furthermore, mitochondria exhibit unstable or oscillatory membrane potentials (ΔΨ_m) when subjected to stress, such as during I/R, but it is unclear if the primary trigger is an excess influx of mitochondrial Ca²⁺ (mCa²⁺), reactive oxygen species (ROS) accumula

SUBMITTER: Ashok D 

PROVIDER: S-EPMC10206190 | biostudies-literature | 2023 Apr

REPOSITORIES: biostudies-literature