Protective role of mitoquinone against impaired mitochondrial homeostasis in metabolic syndrome

Abstract

Mitochondria control various processes in cellular metabolic homeostasis, such as adenosine triphosphate production, generation and clearance of reactive oxygen species, control of intracellular Ca²⁺ and apoptosis, and are thus a critical therapeutic target for metabolic syndrome (MetS). The mitochondrial targeted antioxidant mitoquinone (MitoQ) reduces mitochondrial oxidative stress, prevents impaired mitochondrial dynamics, and increases mitochondrial turnover by promoting autophagy (mitophagy) and mitochondrial biogenesis, which ultimately contribute to the attenuation of MetS conditions, including obesity, insulin resistance, hypertension and cardiovascular disease. The regulatory effect of MitoQ on mitochondrial homeostasis is mediated through AMPK and its downstream signaling pathways, including MTOR, SIRT1, Nrf2 and NF-κB. However, there are few reviews focusing on the critical role of MitoQ as a therapeutic agent in the treatment of MetS. The purpose of this review is to summarize the mitochondrial role in the pathogenesis of MetS, especially in obesity and type 2 diabetes, and discuss the effect and underlying mechanism of MitoQ on mitochondrial homeostasis in MetS.

KEYWORDS:

• Metabolic syndrome
• mitochondria
• mitoquinone
• oxidative stress

Disclosure statement

The authors declare no conflicts of interest.

Additional information

Funding

This study was financial sponsored by Science and Technology Research Program of Chongqing Municipal Education Commission (Grant No. KJQN201900822), Chongqing Engineering Research Center for Processing & Storage of Distinct Agricultural Products (Grant No. KFJJ2019090), Fundamental Research Funds for the Central Universities (Grant No. SWU019026), and Chongqing Technology and Business University (Grant No. 1956024).