Deranged Myocardial Fatty Acid Metabolism in Heart Failure

Yamamoto, Tsunehisa; Sano, Motoaki

doi:10.3390/ijms23020996

Cited by 47 publications

(38 citation statements)

References 143 publications

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“…PPARα-knockout mice have been shown to have a reduced rate of fatty acid oxidation. Interestingly, over-expression of cardiac-specific PPARα significantly reduced enzymes involved in mitochondrial oxidative phosphorylation [43][44][45].…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial-derived Peptide Single-nucleotide Polymorphisms Associated with Cardiovascular Complications in Type 2 Diabetes

Gaona¹,

Gregorio²,

Jiménez³

et al. 2022

Preprint

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Since the discovery of mitochondrial-derived peptides (MDP), their participation in cellular metabolism is no longer considered as the sole function of the mitochondria, but importance was also attached to its role as a source of protective factors of metabolic stress. These peptides are encoded in the mitochondrial genome and translated into the mitochondria or cytoplasm, to signal within the cell or be released and bind to membrane receptors. The objective of this work was explored and compare the frequency of MT-RNR1 and MT-RNR2 variants in sequences obtained from T2D individuals and control population. 213 different mitochondrial polymorphisms previously reported in the literature associated with T2D and cardiovascular diseases were analyzed. We can found three variants in the MT-RNR1 not related with MOTS-c coding sequence: m.1189T>C (rs28358571), m.1420T>C (rs111033356), and m.1438A>G (rs2001030); and secondly, three polymorphisms associated to MT-RNR2 m.2667T>C (rs878870626) related to humanin, m.1811A>G (rs28358576) in SHPL3 and m.3027T>C (rs199838004) in SHPL6 associated with statistical differences between the T2D and control group. All these findings were previously related to cardiovascular complications in literature and, as far as we know, relating for the first time in diabetic patients.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial-derived Peptide Single-nucleotide Polymorphisms Associated with Cardiovascular Complications in Type 2 Diabetes

Gaona¹,

Gregorio²,

Jiménez³

et al. 2022

Preprint

View full text Add to dashboard Cite

show abstract

“…Multiple experimental animal and longitudinal studies have demonstrated that dietinduced obesity promotes pro-aging phenotypes [84,97,171,172]. A considerable component of the obesity-based drive of aging likely results in alterations in insulin sensitivity as well as the drive towards alternative sources of energy, such as lipid-or protein-mediated metabolism that can incur a greater level of oxidative stress [173][174][175].…”

Section: Obesity and Metabolic Dysfunctionmentioning

confidence: 99%

The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease

Leysen

Walter

Clauwaert

et al. 2022

IJMS

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During the aging process our body becomes less well equipped to deal with cellular stress, resulting in an increase in unrepaired damage. This causes varying degrees of impaired functionality and an increased risk of mortality. One of the most effective anti-aging strategies involves interventions that combine simultaneous glucometabolic support with augmented DNA damage protection/repair. Thus, it seems prudent to develop therapeutic strategies that target this combinatorial approach. Studies have shown that the ADP-ribosylation factor (ARF) GTPase activating protein GIT2 (GIT2) acts as a keystone protein in the aging process. GIT2 can control both DNA repair and glucose metabolism. Through in vivo co-regulation analyses it was found that GIT2 forms a close coexpression-based relationship with the relaxin-3 receptor (RXFP3). Cellular RXFP3 expression is directly affected by DNA damage and oxidative stress. Overexpression or stimulation of this receptor, by its endogenous ligand relaxin 3 (RLN3), can regulate the DNA damage response and repair processes. Interestingly, RLN3 is an insulin-like peptide and has been shown to control multiple disease processes linked to aging mechanisms, e.g., anxiety, depression, memory dysfunction, appetite, and anti-apoptotic mechanisms. Here we discuss the molecular mechanisms underlying the various roles of RXFP3/RLN3 signaling in aging and age-related disorders.

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“…That estrogen-related receptor (which main productive molecules promoted by fatty Acyl-COAs productions) is known to regulate a wide range of gene expression in cardiomyocytes, including β-oxidation of FA, oxidative phosphorylation, and contractile proteins [59]. Also, Notes, the generation of Gp GTP subunits is imp for Acyl-COA synthesis (specifically the Gp GTP beta subunits) regulated by OPA1 enzymes in FOX pathway where decreasing in Acyl-COA-beta synthesis will reflect decreasing in both go GTP bêta sublime and in both PLCγ2 and IFN-beta synthesis that will reflect decreasing in the CMs and in ECs activities and functions through dropping in G-actin activities.…”

Section: So the Activation Of The Proper Rac1 In Non-muscle Myosin Lightmentioning

confidence: 99%

Proper Rac1 Required for Ang2 - AT2 Activities for Cardiomyocytes and ECs Where Tyr TAT and TAC Kinases Required for Preventing Glycoprotein Storage and Glycogen Accumulation

Tantawi¹

2022

J Cardiol Res Rev Rep

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Active Rac1 are so imp for improving cytoskeletal systems and necessary for activating IFN-beta & Plcγ2 (which are necessary for regulating TXA2 Synthesis), and are playing imp role for activating CMs and endothelial cells through Ang1 synthesis (mediated by Gp GTP subunits synthesis) then followed by tyrosine kinases function (contain TAT and TAC codons) for Ang2-AT2 productions for adjusting heart contractions and preventing collagen, glycoproteins, and cholesterol accumulations. Angiotensin II type 2 receptors (AT2 receptors) play a modulatory role in blood pressure regulation but produced from Ang1-AT1 by ACE regulated functions , where Tyr codons are playing imp roles in AT1 and AT2 activities and can play so important roles in protecting heart and blood vessels from accumulated cholesterol and glycopeptides and from accumulated glycogen. AT1 receptors promotes the adjustment of various intracellular signaling pathways through Ang2-AT2 production resulting in hypertension, endothelial dysfunction, and recovering the cellular damage.

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Deranged Myocardial Fatty Acid Metabolism in Heart Failure

Cited by 47 publications

References 143 publications

Mitochondrial-derived Peptide Single-nucleotide Polymorphisms Associated with Cardiovascular Complications in Type 2 Diabetes

Mitochondrial-derived Peptide Single-nucleotide Polymorphisms Associated with Cardiovascular Complications in Type 2 Diabetes

The Relaxin-3 Receptor, RXFP3, Is a Modulator of Aging-Related Disease

Proper Rac1 Required for Ang2 - AT2 Activities for Cardiomyocytes and ECs Where Tyr TAT and TAC Kinases Required for Preventing Glycoprotein Storage and Glycogen Accumulation

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