Nuclear-mitochondrial communication involving miR-181c plays an important role in cardiac dysfunction during obesity.

ABSTRACT:

Aims

In cardiomyocytes, there is microRNA (miR) in the mitochondria that originates from the nuclear genome and matures in the cytoplasm before translocating into the mitochondria. Overexpression of one such miR, miR-181c, can lead to heart failure by stimulating reactive oxygen species (ROS) production and increasing mitochondrial calcium level ([Ca²⁺]_m). Mitochondrial calcium uptake 1 protein (MICU1), a regulatory protein in the mitochondrial calcium uniporter complex, plays an important role in regulating [Ca²⁺]_m. Obesity results in miR-181c overexpression and a decrease in MICU1. We hypothesize that lowering miR-181c would protect against obesity-induced cardiac dysfunction.

Methods and results

We used an in vivo mouse model of

SUBMITTER: Roman B 

PROVIDER: S-EPMC7483371 | biostudies-literature | 2020 Jul

REPOSITORIES: biostudies-literature