Maladaptive response following glucose overload in GLUT4‐overexpressing H9C2 cardiomyoblasts

Glucose overload drives diabetic cardiomyopathy by affecting the tricarboxylic acid pathway. However, it is still unknown how cells could overcome massive chronic glucose influx on cellular and structural level.

[1]  Y. Zhang,et al.  Cardiomyocyte-specific knockout of ADAM17 ameliorates left ventricular remodeling and function in diabetic cardiomyopathy of mice , 2022, Signal Transduction and Targeted Therapy.

[2]  P. Riederer,et al.  Neuromelanin granules of the substantia nigra: proteomic profile provides links to tyrosine hydroxylase, stress granules and lysosomes , 2022, Journal of Neural Transmission.

[3]  B. Stratmann,et al.  Chronic Hyperglycaemia Inhibits Tricarboxylic Acid Cycle in Rat Cardiomyoblasts Overexpressing Glucose Transporter Type 4 , 2022, International journal of molecular sciences.

[4]  A. Nestor-Kalinoski,et al.  Intercellular Adhesion Molecule-1 Enhances Myonuclear Transcription during Injury-Induced Muscle Regeneration , 2022, International journal of molecular sciences.

[5]  N. Rabbani.  Methylglyoxal and glyoxalase 1—a metabolic stress pathway-linking hyperglycemia to the unfolded protein response and vascular complications of diabetes , 2022, Clinical science.

[6]  S. Pohl,et al.  Site-1 and site-2 proteases: A team of two in regulated proteolysis. , 2021, Biochimica et biophysica acta. Molecular cell research.

[7]  D. Leroith,et al.  GLUT4-overexpressing engineered muscle constructs as a therapeutic platform to normalize glycemia in diabetic mice , 2021, Science advances.

[8]  N. Bildyug.  Integrins in cardiac hypertrophy: lessons learned from culture systems , 2021, ESC heart failure.

[9]  X. Palomer,et al.  Sirtuins: To Be or Not To Be in Diabetic Cardiomyopathy. , 2021, Trends in molecular medicine.

[10]  Lanfang Li,et al.  Sirtuin 3 Alleviates Diabetic Cardiomyopathy by Regulating TIGAR and Cardiomyocyte Metabolism , 2021, Journal of the American Heart Association.

[11]  P. Pinto-do-Ó,et al.  Bearing My Heart: The Role of Extracellular Matrix on Cardiac Development, Homeostasis, and Injury Response , 2021, Frontiers in Cell and Developmental Biology.

[12]  Wei Liu,et al.  Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside , 2020, Frontiers in Cardiovascular Medicine.

[13]  W. Linke,et al.  The first versatile human iPSC-based model of ectopic virus induction allows new insights in RNA-virus disease , 2020, Scientific Reports.

[14]  M. Irigoyen,et al.  Nicotinamide attenuates streptozotocin-induced diabetes complications and increases survival rate in rats: role of autonomic nervous system , 2020, BMC Endocrine Disorders.

[15]  Chae-Myeong Ha,et al.  Maintaining Myocardial Glucose Utilization in Diabetic Cardiomyopathy Accelerates Mitochondrial Dysfunction , 2020, Diabetes.

[16]  C. Glembotski,et al.  Designing Novel Therapies to Mend Broken Hearts: ATF6 and Cardiac Proteostasis , 2020, Cells.

[17]  J. Krijgsveld,et al.  Human Mast Cell Proteome Reveals Unique Lineage, Putative Functions, and Structural Basis for Cell Ablation. , 2020, Immunity.

[18]  S. Samant,et al.  The nuclear and mitochondrial sirtuins, Sirt6 and Sirt3, regulate each other's activity and protect the heart from developing obesity‐mediated diabetic cardiomyopathy , 2019, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[19]  A. Palazzuoli,et al.  Molecular Dysfunction and Phenotypic Derangement in Diabetic Cardiomyopathy , 2019, International journal of molecular sciences.

[20]  C. Glembotski,et al.  Unfolding the Roles of Mitochondria as Therapeutic Targets for Heart Disease. , 2019, Journal of the American College of Cardiology.

[21]  A. Rojiani,et al.  TIMP-1 downregulation modulates miR-125a-5p expression and triggers the apoptotic pathway , 2018, Oncotarget.

[22]  G. Gonçalves,et al.  Cardiac Hypertrophy and Brain Natriuretic Peptide Levels in an Ovariectomized Rat Model Fed a High-Fat Diet , 2017, Medical science monitor basic research.

[23]  K. Rapti,et al.  Opposite effects of catalase and MnSOD ectopic expression on stress induced defects and mortality in the desmin deficient cardiomyopathy model , 2017, Free radical biology & medicine.

[24]  G. Figtree,et al.  Insulin replacement limits progression of diabetic cardiomyopathy in the low-dose streptozotocin-induced diabetic rat , 2017, Diabetes & vascular disease research.

[25]  Paul J Thornalley,et al.  Intracellular Accumulation of Methylglyoxal by Glyoxalase 1 Knock Down Alters Collagen Homoeostasis in L6 Myoblasts , 2017, International journal of molecular sciences.

[26]  Jüergen Cox,et al.  The MaxQuant computational platform for mass spectrometry-based shotgun proteomics , 2016, Nature Protocols.

[27]  J. Sowers,et al.  Insulin resistance and hyperinsulinaemia in diabetic cardiomyopathy , 2016, Nature Reviews Endocrinology.

[28]  R. Karas,et al.  Intercellular Adhesion Molecule 1 Regulates Left Ventricular Leukocyte Infiltration, Cardiac Remodeling, and Function in Pressure Overload–Induced Heart Failure , 2016, Journal of the American Heart Association.

[29]  M. Giera,et al.  Amino acid analysis using chromatography-mass spectrometry: An inter platform comparison study. , 2015, Journal of pharmaceutical and biomedical analysis.

[30]  Yibin Wang,et al.  A H(a)rd Way to Adapt in Cardiac Hypertrophy. , 2015, Circulation research.

[31]  P. Oliveira,et al.  Gene Expression Profiling of H9c2 Myoblast Differentiation towards a Cardiac-Like Phenotype , 2015, PloS one.

[32]  S. Javadov,et al.  H9c2 and HL-1 cells demonstrate distinct features of energy metabolism, mitochondrial function and sensitivity to hypoxia-reoxygenation. , 2015, Biochimica et biophysica acta.

[33]  Yen-Chung Chen,et al.  Downregulation of Sirt1 as aging change in advanced heart failure , 2014, Journal of Biomedical Science.

[34]  B. Stratmann,et al.  Methylglyoxal Impairs GLUT4 Trafficking and Leads to Increased Glucose Uptake in L6 Myoblasts , 2013, Hormone and Metabolic Research.

[35]  Bernd Stratmann,et al.  Impact of GLO1 Knock Down on GLUT4 Trafficking and Glucose Uptake in L6 Myoblasts , 2013, PloS one.

[36]  M. Selbach,et al.  Global quantification of mammalian gene expression control , 2011, Nature.

[37]  Danica Chen,et al.  Calorie restriction reduces oxidative stress by SIRT3-mediated SOD2 activation. , 2010, Cell metabolism.

[38]  S. Heymans,et al.  TIMPs and cardiac remodeling: 'Embracing the MMP-independent-side of the family'. , 2010, Journal of molecular and cellular cardiology.

[39]  Stephanie L. K. Bowers,et al.  The extracellular matrix: at the center of it all. , 2010, Journal of molecular and cellular cardiology.

[40]  Gene Kim,et al.  Sirt3 blocks the cardiac hypertrophic response by augmenting Foxo3a-dependent antioxidant defense mechanisms in mice. , 2009, The Journal of clinical investigation.

[41]  P. Stiuso,et al.  Exercise training promotes SIRT1 activity in aged rats. , 2008, Rejuvenation research.

[42]  K. Kotani,et al.  Adipose-specific overexpression of GLUT4 reverses insulin resistance and diabetes in mice lacking GLUT4 selectively in muscle. , 2005, American journal of physiology. Endocrinology and metabolism.

[43]  S. Nemoto,et al.  SIRT1 Functionally Interacts with the Metabolic Regulator and Transcriptional Coactivator PGC-1α* , 2005, Journal of Biological Chemistry.

[44]  R. Somwar,et al.  Sustained exposure of L6 myotubes to high glucose and insulin decreases insulin-stimulated GLUT4 translocation but upregulates GLUT4 activity. , 2002, Diabetes.

[45]  M. Shimizu,et al.  Type IV collagen in hypertrophic cardiomyopathy. , 1994, Japanese heart journal.

[46]  S. R. Majeed,et al.  Biochemistry and Molecular Cell Biology of Diabetic Complications , 2020 .

[47]  Xiuhua Wang,et al.  Tissue Inhibitor of Matrix Metalloproteinase-1 Promotes Myocardial Fibrosis by Mediating CD63–Integrin &bgr;1 Interaction , 2017, Hypertension.

[48]  D. Taylor,et al.  Multiple spectral parameter imaging. , 1989, Methods in cell biology.