Cardiometabolic diseases present an escalating global health and economic burden. Such a surge is driven by epidemic prevalence rates of metabolic disorders, such as obesity and type 2 diabetes, and their associated cardiovascular complications, majorly contributing to morbidity and mortality. A fundamental challenge impeding the effective management and therapy of these complications is a lack of clear understanding of the molecular mechanisms underpinning disease initiation and progression. Over the past decade, a role for metabolic disease-associated adipose tissue dysfunction and inflammation in evoking cardiovascular and renal deterioration emerged, together with a growing recognition of the positive impact of pharmacological tools modulating adipose tissue function. Adipose tissue is a plastic endocrine organ whose homeostasis is essentially dependent on the intercellular communication of its comprising cellular components. Yet, despite being a principal regulator of adipose tissue metabolic activity, changes in aspects of adipose tissue mitochondrial biogenesis, dynamics, and bioenergetics in the context of cardiometabolic disorders have not garnered the necessary attention. Here, we gather the available evidence on the contribution of mitochondrial dysfunction to that of the adipose tissue in metabolic diseases, and to the ensuing cardiovascular deterioration. The involved molecular pathways are highlighted together with potential targets for intervention. The effects of several drug classes with known beneficial impact on adipose tissue remodeling and mitochondrial dysfunction in such a context are discussed. Finally, future research aspects in this domain are explored.
Keywords: Adipose; Cardiovascular disease; Metabolic disease; Mitochondria; UCP1.
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