Tags

Type your tag names separated by a space and hit enter

An overview of the crosstalk between inflammatory processes and metabolic dysregulation during diabetic cardiomyopathy.

Abstract

Metabolic disorders such as obesity, insulin resistance and type 2 diabetes mellitus are all linked to cardiovascular diseases such as cardiac hypertrophy and heart failure. Diabetic cardiomyopathy in particular, is characterized by structural and functional alterations in the heart muscle of people with diabetes that finally lead to heart failure, and which is not directly attributable to coronary artery disease or hypertension. Several mechanisms have been involved in the pathogenesis of diabetic cardiomyopathy, such as alterations in myocardial energy metabolism and calcium signaling. Metabolic disturbances during diabetic cardiomyopathy are characterized by increased lipid oxidation, intramyocardial triglyceride accumulation, and reduced glucose utilization. Overall changes result in enhanced oxidative stress, mitochondrial dysfunction and apoptosis of the cardiomyocytes. On the other hand, the progression of heart failure and cardiac hypertrophy usually entails a local rise in cytokines in cardiac cells and the activation of the proinflammatory transcription factor nuclear factor (NF)-κB. Interestingly, increasing evidences are arising in the recent years that point to a potential link between chronic low-grade inflammation in the heart and metabolic dysregulation. Therefore, in this review we summarize recent new insights into the crosstalk between inflammatory processes and metabolic dysregulation in the failing heart during diabetes, paying special attention to the role of NF-κB and peroxisome proliferator activated receptors (PPARs). In addition, we briefly describe the role of the AMP-activated protein kinase (AMPK), sirtuin 1 (SIRT1) and other pathways regulating cardiac energy metabolism, as well as their relationship with diabetic cardiomyopathy.

Links

  • Publisher Full Text
  • Authors+Show Affiliations

    ,

    Department of Pharmacology and Therapeutic Chemistry, IBUB (Institut de Biomedicina de la Universitat de Barcelona), Spain; CIBER de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Faculty of Pharmacy, University of Barcelona, Diagonal 643, Barcelona E-08028, Spain.

    , ,

    Source

    International journal of cardiology 168:4 2013 Oct 09 pg 3160-72

    MeSH

    Animals
    Diabetic Cardiomyopathies
    Energy Metabolism
    Glucose
    Humans
    Inflammation
    Insulin
    Lipid Metabolism
    Signal Transduction

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    23932046

    Citation

    Palomer, Xavier, et al. "An Overview of the Crosstalk Between Inflammatory Processes and Metabolic Dysregulation During Diabetic Cardiomyopathy." International Journal of Cardiology, vol. 168, no. 4, 2013, pp. 3160-72.
    Palomer X, Salvadó L, Barroso E, et al. An overview of the crosstalk between inflammatory processes and metabolic dysregulation during diabetic cardiomyopathy. Int J Cardiol. 2013;168(4):3160-72.
    Palomer, X., Salvadó, L., Barroso, E., & Vázquez-Carrera, M. (2013). An overview of the crosstalk between inflammatory processes and metabolic dysregulation during diabetic cardiomyopathy. International Journal of Cardiology, 168(4), pp. 3160-72. doi:10.1016/j.ijcard.2013.07.150.
    Palomer X, et al. An Overview of the Crosstalk Between Inflammatory Processes and Metabolic Dysregulation During Diabetic Cardiomyopathy. Int J Cardiol. 2013 Oct 9;168(4):3160-72. PubMed PMID: 23932046.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - An overview of the crosstalk between inflammatory processes and metabolic dysregulation during diabetic cardiomyopathy. AU - Palomer,Xavier, AU - Salvadó,Laia, AU - Barroso,Emma, AU - Vázquez-Carrera,Manuel, Y1 - 2013/08/06/ PY - 2013/06/06/received PY - 2013/07/15/accepted PY - 2013/8/13/entrez PY - 2013/8/13/pubmed PY - 2014/6/27/medline KW - ACO KW - ACS KW - AMP-activated protein kinase KW - AMPK KW - CPT KW - Cardiovascular Disease KW - ERK1/2 KW - ERR KW - FABP KW - FAT/CD36 KW - FATP KW - FOXO1 KW - Heart KW - IKK KW - IL-6 KW - Inflammation KW - IκB kinase KW - JNK KW - LDL KW - LPL KW - MAPK KW - MCAD KW - MCP-1 KW - Metabolism KW - NADH KW - NF-κB KW - NFAT KW - PDC KW - PDK KW - PGC-1α KW - PI3K KW - PKB/Akt KW - PPAR KW - PPRE KW - ROS KW - RXR KW - SAFE KW - SIRT1 KW - SOCS KW - STAT KW - TCA KW - TNF-α KW - acyl-CoA oxidase KW - acyl-CoA synthase KW - c-Jun N-terminal kinase KW - calcineurin-nuclear factor of activated T cells KW - carnitine palmitoyl transferase KW - estrogen-related receptor KW - extracellular signal-regulated protein kinase 1/2 KW - fatty acid binding protein KW - fatty acid translocase/CD36 KW - fatty acid transport protein KW - forkhead transcription factor KW - interleukin 6 KW - lipoprotein lipase KW - low density lipoprotein KW - medium-chain acyl-CoA dehydrogenase KW - mitogen-activated protein kinase KW - monocyte chemoattractant protein-1 KW - nicotinamide adenine dinucleotide KW - nuclear factor-κB KW - peroxisome proliferator response element KW - peroxisome proliferator-activated receptor KW - peroxisome proliferator-activated receptor γ coactivator-1α KW - phosphatidylinositol 3 kinase KW - protein kinase B KW - pyruvate dehydrogenase complex KW - pyruvate dehydrogenase kinase KW - reactive oxygen species KW - retinoid X receptor KW - signal transducer and activator of transcription KW - sirtuin 1 KW - suppressor of cytokine signaling KW - survival activating factor enhancement KW - tricarboxylic acid cycle KW - tumor necrosis factor-α SP - 3160 EP - 72 JF - International journal of cardiology JO - Int. J. Cardiol. VL - 168 IS - 4 N2 - Metabolic disorders such as obesity, insulin resistance and type 2 diabetes mellitus are all linked to cardiovascular diseases such as cardiac hypertrophy and heart failure. Diabetic cardiomyopathy in particular, is characterized by structural and functional alterations in the heart muscle of people with diabetes that finally lead to heart failure, and which is not directly attributable to coronary artery disease or hypertension. Several mechanisms have been involved in the pathogenesis of diabetic cardiomyopathy, such as alterations in myocardial energy metabolism and calcium signaling. Metabolic disturbances during diabetic cardiomyopathy are characterized by increased lipid oxidation, intramyocardial triglyceride accumulation, and reduced glucose utilization. Overall changes result in enhanced oxidative stress, mitochondrial dysfunction and apoptosis of the cardiomyocytes. On the other hand, the progression of heart failure and cardiac hypertrophy usually entails a local rise in cytokines in cardiac cells and the activation of the proinflammatory transcription factor nuclear factor (NF)-κB. Interestingly, increasing evidences are arising in the recent years that point to a potential link between chronic low-grade inflammation in the heart and metabolic dysregulation. Therefore, in this review we summarize recent new insights into the crosstalk between inflammatory processes and metabolic dysregulation in the failing heart during diabetes, paying special attention to the role of NF-κB and peroxisome proliferator activated receptors (PPARs). In addition, we briefly describe the role of the AMP-activated protein kinase (AMPK), sirtuin 1 (SIRT1) and other pathways regulating cardiac energy metabolism, as well as their relationship with diabetic cardiomyopathy. SN - 1874-1754 UR - https://www.unboundmedicine.com/medline/citation/23932046/An_overview_of_the_crosstalk_between_inflammatory_processes_and_metabolic_dysregulation_during_diabetic_cardiomyopathy_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0167-5273(13)01361-2 DB - PRIME DP - Unbound Medicine ER -