Molecular Perspectives of Mitochondrial Adaptations and Their Role in Cardiac Proteostasis

Alam, Shariful; Abdullah, Chowdhury S.; Aishwarya, Richa; Morshed, Mahboob; Bhuiyan, Md. Shenuarin

doi:10.3389/fphys.2020.01054

Cited by 6 publications

(3 citation statements)

References 201 publications

(242 reference statements)

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“…In response to signals from these sensors, mitochondria can respond by changing the balance of mitochondrial fission and fusion, undergoing mitochondrial biogenesis, and/or initiating mitophagy to remove dysfunctional mitochondria. These mitochondrial morphologic changes have effects downstream by changing the oxidative capacity, mitochondrial membrane potential, and reactive oxygen species (ROS) levels to control cardiomyocyte phenotype [22]. We will discuss each of these further in the context of the different metabolic transitions below but briefly review their role in mitochondrial dynamics and function here.…”

Section: Overview Of Molecular Sensors and Mitochondrial Responsesmentioning

confidence: 99%

Mitochondria and metabolic transitions in cardiomyocytes: lessons from development for stem cell-derived cardiomyocytes

Garbern

Lee

2021

Stem Cell Res Ther

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Current methods to differentiate cardiomyocytes from human pluripotent stem cells (PSCs) inadequately recapitulate complete development and result in PSC-derived cardiomyocytes (PSC-CMs) with an immature or fetal-like phenotype. Embryonic and fetal development are highly dynamic periods during which the developing embryo or fetus is exposed to changing nutrient, oxygen, and hormone levels until birth. It is becoming increasingly apparent that these metabolic changes initiate developmental processes to mature cardiomyocytes. Mitochondria are central to these changes, responding to these metabolic changes and transitioning from small, fragmented mitochondria to large organelles capable of producing enough ATP to support the contractile function of the heart. These changes in mitochondria may not simply be a response to cardiomyocyte maturation; the metabolic signals that occur throughout development may actually be central to the maturation process in cardiomyocytes. Here, we review methods to enhance maturation of PSC-CMs and highlight evidence from development indicating the key roles that mitochondria play during cardiomyocyte maturation. We evaluate metabolic transitions that occur during development and how these affect molecular nutrient sensors, discuss how regulation of nutrient sensing pathways affect mitochondrial dynamics and function, and explore how changes in mitochondrial function can affect metabolite production, the cell cycle, and epigenetics to influence maturation of cardiomyocytes.

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Section: Overview Of Molecular Sensors and Mitochondrial Responsesmentioning

confidence: 99%

Mitochondria and metabolic transitions in cardiomyocytes: lessons from development for stem cell-derived cardiomyocytes

Garbern

Lee

2021

Stem Cell Res Ther

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“…Even if we did not analyze autophagy in the heart here, in the liver of HET mice, we documented inconsistent autophagy already in basal conditions [54]. Furthermore, accelerated senescence has been reported in cardiac hypertrophy in mice defective in mitochondrial shaping proteins [80], and lipofuscins correlate with mitochondria swelling in HET mice, as indicated by Alam et al [26].…”

Section: Discussionmentioning

confidence: 62%

“…Mitochondria represent up to 45% of a single cardiomyocyte volume and are scattered in different subcellular sites and so defined as subsarcolemmal, inter-myofibrillar (IMF), and perinuclear populations [25]. Despite the forced regular presence of mitochondria in the sarcomere, their dynamism and ability to change size are essential to maintaining energetic metabolism in the heart [26,27]. Indeed, the prevalence of small mitochondria, called fission, or elongated mitochondria, called fusion, may be detrimental or beneficial for ATP production [28] and precedes reactive oxygen species production [29].…”

Section: Of 19mentioning

confidence: 99%

Cardiometabolic Changes in Sirtuin1-Heterozygous Mice on High-Fat Diet and Melatonin Supplementation

Favero,

Golic,

Arnaboldi

et al. 2024

IJMS

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A hypercaloric fatty diet predisposes an individual to metabolic syndrome and cardiovascular complications. Sirtuin1 (SIRT1) belongs to the class III histone deacetylase family and sustains anabolism, mitochondrial biogenesis, and fat distribution. Epididymal white adipose tissue (eWAT) is involved in inflammation, whilst interscapular brown adipose tissue (iBAT) drives metabolism in obese rodents. Melatonin, a pineal indoleamine, acting as a SIRT1 modulator, may alleviate cardiometabolic damage. In the present study, we morphologically characterized the heart, eWAT, and iBAT in male heterozygous SIRT1+/− mice (HET mice) on a high-fat diet (60%E lard) versus a standard rodent diet (8.5% E fat) and drinking melatonin (10 mg/kg) for 16 weeks. Wild-type (WT) male C57Bl6/J mice were similarly fed for comparison. Cardiomyocyte fibrosis and endoplasmic reticulum (ER) stress response worsened in HET mice on a high-fat diet vs. other groups. Lipid peroxidation, ER, and mitochondrial stress were assessed by 4 hydroxy-2-nonenal (4HNE), glucose-regulated protein78 (GRP78), CCAA/enhancer-binding protein homologous protein (CHOP), heat shock protein 60 (HSP60), and mitofusin2 immunostainings. Ultrastructural analysis indicated the prevalence of atypical inter-myofibrillar mitochondria with short, misaligned cristae in HET mice on a lard diet despite melatonin supplementation. Abnormal eWAT adipocytes, crown-like inflammatory structures, tumor necrosis factor alpha (TNFα), and iBAT whitening characterized HET mice on a hypercaloric fatty diet and were maintained after melatonin supply. All these data suggest that melatonin’s mechanism of action is strictly linked to full SIRT1 expression, which is required for the exhibition of effective antioxidant and anti-inflammatory properties.

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Comprehensive Multi-omics Analysis Reveals Mitochondrial Stress as a Central Biological Hub for Spaceflight Impact

Silveira

Fazelinia

Rosenthal

et al. 2020

Cell

184

191

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Molecular Perspectives of Mitochondrial Adaptations and Their Role in Cardiac Proteostasis

Cited by 6 publications

References 201 publications

Mitochondria and metabolic transitions in cardiomyocytes: lessons from development for stem cell-derived cardiomyocytes

Mitochondria and metabolic transitions in cardiomyocytes: lessons from development for stem cell-derived cardiomyocytes

Cardiometabolic Changes in Sirtuin1-Heterozygous Mice on High-Fat Diet and Melatonin Supplementation

Comprehensive Multi-omics Analysis Reveals Mitochondrial Stress as a Central Biological Hub for Spaceflight Impact

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