Abstract
Heart failure (HF) frequently coexists with conditions associated with glucose insufficiency, such as insulin resistance and type 2 diabetes mellitus (T2DM), and patients with T2DM have a significantly high incidence of HF. These two closely related diseases cannot be separated on the basis of their treatment. Some antidiabetic drugs failed to improve cardiac outcomes in T2DM patients, despite lowering glucose levels sufficiently. This may be, at least in part, due to a lack of understanding of cardiac insulin resistance. Basic investigations have revealed the significant contribution of cardiac insulin resistance to the pathogenesis and progression of HF; however, there is no clinical evidence of the definition or treatment of cardiac insulin resistance. Mitochondrial dynamics play an important role in cardiac insulin resistance and HF because they maintain cellular homeostasis through energy production, cell survival, and cell proliferation. The innovation of diagnostic tools and/or treatment targeting mitochondrial dynamics is assumed to improve not only the insulin sensitivity of the myocardium and cardiac metabolism, but also the cardiac contraction function. In this review, we summarized the current knowledge on the correlation between cardiac insulin resistance and progression of HF, and discussed the role of mitochondrial dynamics on the pathogenesis of cardiac insulin resistance and HF. We further discuss the possibility of mitochondria-targeted intervention to improve cardiac metabolism and HF.
Highlights
Heart failure (HF) is a condition in which the myocardium is unable to meet the whole body’s demand for blood and oxygen and is caused by complex and multiple factors
HF frequently coexists with conditions associated with glucose insufficiency, such as insulin resistance or type 2 diabetes mellitus (T2DM), and T2DM patients have a higher incidence of HF than normal subjects
HF frequently coexists with glucose insufficiency such as T2DM and insulin resistance
Summary
Heart failure (HF) is a condition in which the myocardium is unable to meet the whole body’s demand for blood and oxygen and is caused by complex and multiple factors. The intensive glucose lowering therapy cannot always improve the prognosis of T2DM patients [2], and some antidiabetic drugs failed to improve cardiac outcomes in T2DM patients, despite sufficiently lowering glucose levels [2] This may be due to a lack of understanding and/or knowledge of cardiac insulin resistance. Cardiac insulin resistance is considered to develop independently of systemic insulin resistance, the alterations due to systemic insulin resistance, such as overnutrition, oxidative stress, neurohormonal imbalance and increased cytokines significantly contribute to the promotion of cardiac insulin resistance [3]. In this basic research field, there is obvious evidence that cardiac insulin resistance significantly contributes to the pathogenesis and progression of HF [4]. We summarize the current knowledge regarding the relationship between cardiac insulin resistance and the dysregulation of mitochondrial dynamics in patients with HF and discuss the possibility of a mitochondria-targeted diagnosis and interventions in cardiac insulin resistance
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