Thyroid Stimulating Hormone Triggers Hepatic Mitochondrial Stress through Cyclophilin D Acetylation

Abstract

Background & aims: Oxidative stress-related liver diseases were shown to be associated with elevated serum thyroid stimulating hormone (TSH) levels. Mitochondria are the main source of cellular reactive oxygen species. However, the relationship between TSH and hepatic mitochondrial stress/dysfunction and the underlying mechanisms are largely unknown. Here, we focused on exploring the effects and mechanism of TSH on hepatic mitochondrial stress.

Methods: As the function of TSH is mediated through the TSH receptor (TSHR), Tshr ^-/- mice and liver-specific Tshr ^-/- mice and liver-specific Tshr ^-/- mice and liver-specific.

Results: A relatively lower degree of mitochondrial stress was observed in the livers of Tshr ^-/- mice and liver-specific in vitro. Microarray and RT-PCR analyses showed that Tshr ^-/- mice and liver-specific.

Conclusions: TSH stimulates hepatic CypD acetylation through the lncRNA-AK044604/SIRT1/SIRT3 signaling pathway, indicating an essential role for TSH in mitochondrial stress in the liver.