Abstract
Chronic hypoxia is an essential component in many cardiac diseases. The heart consumes a substantial amount of energy and it is important to maintain the balance of energy supply and demand when oxygen is limited. Previous studies showed that the heart switches from fatty acid to glucose to maintain metabolic efficiency in the adaptation to chronic hypoxia. However, the underlying mechanism of this adaptive cardiac metabolism remains to be fully characterized. Moreover, how the altered cardiac metabolism affects the heart function in patients with chronic hypoxia has not been discussed in the current literature. In this review, we summarized new findings from animal and human studies to illustrate the mechanism underlying the adaptive cardiac metabolism under chronic hypoxia. Clinical focus is given to certain patients that are subject to the impact of chronic hypoxia, and potential treatment strategies that modulate cardiac metabolism and may improve the heart function in these patients are also summarized.
Highlights
The human heart is extremely robust in energy metabolism with the highest uptake of oxygen in the body (∼0.1 ml O2/g/min), and requires ∼6 kg of ATP per day, which is 15–20 times its own weight (Kolwicz et al, 2013)
chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) can lead to chronic systemic hypoxia in affected patients, whereas obstructive sleep apnea (OSA) is associated with another type of chronic hypoxia that is characterized by recurrent episodes of hypoxia and reoxygenation, i.e., chronic intermittent hypoxia (CIH)
In rats exposed to chronic hypoxia for 3 weeks, reduced cardiac expression of cold-inducible RNA binding protein (CIRBP) caused decreased stabilization of the mRNA responsible for the biosynthesis of Coenzyme Q10 (CoQ10), which could be associated with reduced ATP production, increased cellular apoptosis, and impaired heart function upon acute stress (Liu et al, 2019)
Summary
The human heart is extremely robust in energy metabolism with the highest uptake of oxygen in the body (∼0.1 ml O2/g/min), and requires ∼6 kg of ATP per day, which is 15–20 times its own weight (Kolwicz et al, 2013). The heart is challenged to produce similar amount of ATP with limited O2 for contractile work to maintain normal heart function. This comes in the issue of cardiac metabolic efficiency, which is important in heart function as impaired metabolic efficiency appears to be a prominent feature in heart failure (Bertero and Maack, 2018). In response to hypoxic stimuli, the heart has evolved a delicate adaptive program to maintain metabolic efficiency, in which glucose becomes preferentially used over fatty acid for ATP production. Cardiac Metabolism Under Chronic Hypoxia when glucose utilization is increased, the coupling of glycolysis and glucose oxidation improves cardiac metabolic efficiency and maintains ATP production (Abdurrachim et al, 2015). The role of altered metabolic adaptation in the progression of cardiac dysfunction in patients with chronic hypoxia and potential available treatment strategies are discussed
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