Mitochondrial Dysfunction in Metabolic Diseases

Mitochondria are crucial bioenergetic powerhouses and biosynthetic hubs within cells, which can generate and sequester toxic reactive oxygen species (ROS) in response to oxidative stress. Oxidative stress-stimulated ROS production can result in ATP depletion and the opening of mitochondrial permeability transition pores, leading to mitochondria dysfunction and cellular apoptosis. Mitochondrial loss of function is also a key driver in the acquisition of a senescence-associated secretory phenotype that drives senescent cells into a pro-inflammatory state. Emerging evidence suggests that mitochondrial dysfunction plays a direct role in metabolic disorders including ischemia-reperfusion (I/R) injury, hypertension, lipodystrophy, diabetes, cardiac hypertrophy, heart failure, calcific aortic valve disease, atherosclerosis, amyotrophic lateral sclerosis and chronic kidney disease. The key players underpinning mitochondrial dysfunction are ROS, REDOX balance, the Krebs cycle and the oxidative phosphorylation machinery, the mitochondrial membrane polarization, calcium regulation, the imbalance of mitochondrial fission and fusion, dysregulated mitophagy, mitochondrial DNA mutations and perturbations in the mitochondrial unfolded protein response. Early control of mitochondrial dysfunction could thus be a crucial step in the therapeutic control of metabolic diseases.

Mitochondrial dysfunction in metabolic diseases is a fast-emerging area of research and holds great promise for future therapies. We would like to make a unique collection of articles, which underpins all the aspects of mitochondrial dysfunction in major metabolic disorders along with recent advances in mitochondria based therapeutic strategies. This will include the key molecular players with a role in causing mitochondrial dysfunction and the consequences thereof, the effect of mitochondrial dysfunction on the metabolic machinery, the role of mitochondrial DNA, mitochondrial fusion and fission, mitochondrial protein synthesis, mitochondrial dysfunction-related inflammation and senescence-associated secretory phenotype and finally the role of selective clearance of damaged mitochondria by mitophagy in these diseases. The research topic will also highlight currently available cellular and animal models and will discuss novel potential models which can be developed to study mitochondrial dysfunction in major metabolic disorders.
We welcome articles which cover current trends in the field along with providing broad understanding of the topic.

Areas to cover may include:
• Mitochondrial damage in vascular calcification diseases;
• Role of mitophagy in metabolic diseases;
• Role of mitochondria in senescence in metabolic diseases;
• Mitochondrial damage and mitophagy in chronic kidney disease, vascular and valvular diseases, type –II diabetes and obesity;
• Mitochondrial translation defects in metabolic diseases;
• Mitochondrial DNA mutations in metabolic diseases;
• Mitochondrial ROS in metabolic diseases;
• Mitochondrial bioenergetics failure in metabolic diseases;
• Mitochondria based therapeutic strategies in metabolic diseases;
• Imaging advances/novel tools to study and detect mitochondrial damage in metabolic diseases;
• Mitoproteome in metabolic diseases.