The mechanism of 14-3-3η in thyroxine induced mitophagy in cardiomyocytes.

Hyperthyroidism is becoming increasingly important as an independent risk factor for cardiovascular disease, eventually resulting in cardiac hypertrophy and heart failure. The 14-3-3 protein family subtypes regulate many cellular processes in eukaryotes by interacting with a diverse array of client proteins. Considering that the 14-3-3η protein protects cardiomyocytes by affecting mitochondrial function, exploring the biological influence and molecular mechanisms by which 14-3-3η alleviates the cardiac hypertrophy of hyperthyroidism is imperative.

Correction to: miR-762 modulates thyroxine-induced cardiomyocyte hypertrophy by inhibiting Beclin-1.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

miR-762 modulates thyroxine-induced cardiomyocyte hypertrophy by inhibiting Beclin-1.

Purpose: Whether autophagy plays a key role in thyroxine-induced cardiomyocyte hypertrophy, and whether the role of autophagy in thyroxine-induced cardiomyocyte hypertrophy is related to targeting of Beclin-1 by miR-762 remains unclear. This research focused on testing these two hypotheses. Importantly, the results of this study will help us better understand the molecular mechanisms of thyroxine-induced cardiomyocyte hypertrophy.

Mutant huntingtin inhibits the mitochondrial unfolded protein response by impairing ABCB10 mRNA stability.

Numerous studies have shown that mitochondrial dysfunction contributes to consequential phenotypes of Huntington's disease (HD), a fatal and inherited neurodegenerative disease caused by the expanded CAG repeats in the N-terminus of the huntingtin (Htt) gene. To maintain proper function, mitochondria develop a dedicated protein quality control mechanism by activating a stress response termed the mitochondrial unfolded protein response (UPR). Defects in the UPR have been linked to aging and are also associated with neurodegenerative diseases.