Influence fatty acids on oxygen consumption by isolated rat cardiomyocytes in ischemic or diabetic heart disease

Sa, Afanasiev; Mv, Egorova; Tv, Kutsykova; Попов, С. В.

doi:10.15690/vramn612

Cited by 4 publications

(5 citation statements)

References 5 publications

(8 reference statements)

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“…12 Cardiomyocytes are particularly susceptible to diabetic insults caused by dysfunctional mitochondria. 13,14 Mitochondria that are damaged during diabetic stress can produce reactive oxygen species (ROS) and release death-inducing factors, thus augmenting cardiomyocyte injury. [14][15][16] Effective clearance of these damaged mitochondria may prevent cardiomyocyte damage induced by diabetes and limit cardiac dysfunction.…”

Section: Introductionmentioning

confidence: 99%

“…13,14 Mitochondria that are damaged during diabetic stress can produce reactive oxygen species (ROS) and release death-inducing factors, thus augmenting cardiomyocyte injury. [14][15][16] Effective clearance of these damaged mitochondria may prevent cardiomyocyte damage induced by diabetes and limit cardiac dysfunction. 13,17 Autophagy is the primary mechanism for mitochondrial quality control and removes whole mitochondria.…”

Section: Introductionmentioning

confidence: 99%

“…Increasing evidence suggests that the cardiovascular complications of diabetes converge on mitochondria as an epicentre for cardiomyocyte damage . Cardiomyocytes are particularly susceptible to diabetic insults caused by dysfunctional mitochondria . Mitochondria that are damaged during diabetic stress can produce reactive oxygen species (ROS) and release death‐inducing factors, thus augmenting cardiomyocyte injury …”

Section: Introductionmentioning

confidence: 99%

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Melatonin activates Parkin translocation and rescues the impaired mitophagy activity of diabetic cardiomyopathy through Mst1 inhibition

Wang

Zhao

Feng

et al. 2018

J Cellular Molecular Medi

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Mitophagy eliminates dysfunctional mitochondria and thus plays a cardinal role in diabetic cardiomyopathy (DCM). We observed the favourable effects of melatonin on cardiomyocyte mitophagy in mice with DCM and elucidated their underlying mechanisms. Electron microscopy and flow cytometric analysis revealed that melatonin reduced the number of impaired mitochondria in the diabetic heart. Other than decreasing mitochondrial biogenesis, melatonin increased the clearance of dysfunctional mitochondria in mice with DCM. Melatonin increased LC3 II expression as well as the colocalization of mitochondria and lysosomes in HG‐treated cardiomyocytes and the number of typical autophagosomes engulfing mitochondria in the DCM heart. These results indicated that melatonin promoted mitophagy. When probing the mechanism, increased Parkin translocation to the mitochondria may be responsible for the up‐regulated mitophagy exerted by melatonin. Parkin knockout counteracted the beneficial effects of melatonin on the cardiac mitochondrial morphology and bioenergetic disorders, thus abolishing the substantial effects of melatonin on cardiac remodelling with DCM. Furthermore, melatonin inhibited Mammalian sterile 20‐like kinase 1 (Mst1) phosphorylation, thus enhancing Parkin‐mediated mitophagy, which contributed to mitochondrial quality control. In summary, this study confirms that melatonin rescues the impaired mitophagy activity of DCM. The underlying mechanism may be attributed to activation of Parkin translocation via inhibition of Mst1.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Melatonin activates Parkin translocation and rescues the impaired mitophagy activity of diabetic cardiomyopathy through Mst1 inhibition

Wang

Zhao

Feng

et al. 2018

J Cellular Molecular Medi

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“…For 1 mole of an unsaturated long-chain fatty acids like palmitate, the net energy production is estimated at 128 ATP, whereas this rate reaches at only 38 ATP for 1 mole of glucose (Stanley et al, 1997 ). However, in comparison to glycolysis, FAO uses 12% more dioxygen and thus FAO is considered less dioxygen-efficient (Mjos, 1971 ; Grynberg and Demaison, 1996 ; Afanasiev et al, 2016 ). Consequently, even a major component of cardiac energy production, FAO is thus particularly sensitive to dioxygen concentration, and a tight equilibrium must be kept between availability of fuel sources.…”

Section: Lability and Physiological Adaptation Within The Heartmentioning

confidence: 99%

Dioxygen and Metabolism; Dangerous Liaisons in Cardiac Function and Disease

Angelini

Xie

2017

Front. Physiol.

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The heart must consume a significant amount of energy to sustain its contractile activity. Although the fuel demands are huge, the stock remains very low. Thus, in order to supply its daily needs, the heart must have amazing adaptive abilities, which are dependent on dioxygen availability. However, in myriad cardiovascular diseases, “fuel” depletion and hypoxia are common features, leading cardiomyocytes to favor low-dioxygen-consuming glycolysis rather than oxidation of fatty acids. This metabolic switch makes it challenging to distinguish causes from consequences in cardiac pathologies. Finally, despite the progress achieved in the past few decades, medical treatments have not improved substantially, either. In such a situation, it seems clear that much remains to be learned about cardiac diseases. Therefore, in this review, we will discuss how reconciling dioxygen availability and cardiac metabolic adaptations may contribute to develop full and innovative strategies from bench to bedside.

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“…The cohort study VALIANT has showed that T2DM is an independent predictor of unfavorable coronary events during the first year after myocardial infarction or patient death [4]. Our previous studies showed that CHD and T2DM comorbidity significantly affects cardiac remodeling at the cellular and molecular levels [1,2,5]. The combined influence of ischemic and diabetic/hyperglycemic factors on the cardiac muscle was also demonstrated in biologic models and in patients with comorbidity.…”

mentioning

confidence: 96%

Expression of Genes and Proteins of the Sarcoplasmic Reticulum Са2+-Transport Systems in Cardiomyocytes in Concomitant Coronary Heart Disease and Type 2 Diabetes Mellitus

et al. 2021

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We compared the expression of Са 2+ -ATPase (SERCA2a), calsequestrin (CASQ2), ryanodine receptors (RyR2) proteins and their genes (ATP2A2, CASQ2, and RYR2) in coronary heart disease (CHD) patients with and without comorbid type 2 diabetes mellitus. All studies were performed on the right atrial appendages resected during coronary bypass surgeries. Expression of SERCA2a and RyR2 proteins and their ATP2A2 (p=0.046) and RYR2 genes in comorbid pathology was significantly (p=0.042) higher (by 1.2 and 2 times; p=0.025). The expression of CASQ2 protein and its gene did not differ significantly between the groups (p=0.82 and p=0.066, respectively). It was concluded that the expression of SERCA2a and RyR2 proteins and their genes (but not CASQ2 and its gene) is elevated in CHD associated with type 2 diabetes mellitus. Expression of the studied proteins correlated with the expression of their genes. Increased expression of CASQ2 protein and its gene can probably prevent imbalance of the Ca 2+ -transporting systems in cardiomyocytes and contractile dysfunction of the myocardium, even in CHD associated with type 2 diabetes mellitus.

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Influence fatty acids on oxygen consumption by isolated rat cardiomyocytes in ischemic or diabetic heart disease

Cited by 4 publications

References 5 publications

Melatonin activates Parkin translocation and rescues the impaired mitophagy activity of diabetic cardiomyopathy through Mst1 inhibition

Melatonin activates Parkin translocation and rescues the impaired mitophagy activity of diabetic cardiomyopathy through Mst1 inhibition

Dioxygen and Metabolism; Dangerous Liaisons in Cardiac Function and Disease

Expression of Genes and Proteins of the Sarcoplasmic Reticulum Са2+-Transport Systems in Cardiomyocytes in Concomitant Coronary Heart Disease and Type 2 Diabetes Mellitus

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