Extracellular microRNAs and endothelial hyperglycaemic memory: a therapeutic opportunity?
Type 2 diabetes mellitus (T2DM) is a major cause of cardiovascular (CV) disease. Several large clinical trials have shown that the risk for patients with diabetes of developing CV complications is only partially reduced by early, intensive glycaemic control and lifestyle interventions, and that such...
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| Published in | Diabetes, obesity & metabolism Vol. 18; no. 9; pp. 855 - 867 |
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| Main Authors | , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Oxford, UK
Blackwell Publishing Ltd
01.09.2016
Wiley Subscription Services, Inc |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1462-8902 1463-1326 1463-1326 |
| DOI | 10.1111/dom.12688 |
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| Abstract | Type 2 diabetes mellitus (T2DM) is a major cause of cardiovascular (CV) disease. Several large clinical trials have shown that the risk for patients with diabetes of developing CV complications is only partially reduced by early, intensive glycaemic control and lifestyle interventions, and that such complications result from changes in complex, not fully explored networks that contribute to the maintenance of endothelial function. The accumulation of senescent cells and the low‐grade, systemic, inflammatory status that accompanies aging (inflammaging) are involved in the development of endothelial dysfunction. Such phenomena are modulated by epigenetic mechanisms, including microRNAs (miRNAs). MiRNAs can modulate virtually all gene transcripts. They can be secreted by living cells and taken up in active form by recipient cells, providing a new communication tool between tissues and organs. MiRNA deregulation has been associated with the development and progression of a number of age‐related diseases, including the enduring gene expression changes seen in patients with diabetes. We review recent evidence on miRNA changes in T2DM, focusing on the ability of diabetes‐associated miRNAs to modulate endothelial function, inflammaging and cellular senescence. We also discuss the hypothesis that miRNA‐containing extracellular vesicles (i.e. exosomes and microvesicles) could be harnessed to restore a ‘physiological’ signature capable of preventing or delaying the harmful systemic effects of T2DM. |
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| AbstractList | Type 2 diabetes mellitus (T2DM) is a major cause of cardiovascular (CV) disease. Several large clinical trials have shown that the risk for patients with diabetes of developing CV complications is only partially reduced by early, intensive glycaemic control and lifestyle interventions, and that such complications result from changes in complex, not fully explored networks that contribute to the maintenance of endothelial function. The accumulation of senescent cells and the low-grade, systemic, inflammatory status that accompanies aging (inflammaging) are involved in the development of endothelial dysfunction. Such phenomena are modulated by epigenetic mechanisms, including microRNAs (miRNAs). MiRNAs can modulate virtually all gene transcripts. They can be secreted by living cells and taken up in active form by recipient cells, providing a new communication tool between tissues and organs. MiRNA deregulation has been associated with the development and progression of a number of age-related diseases, including the enduring gene expression changes seen in patients with diabetes. We review recent evidence on miRNA changes in T2DM, focusing on the ability of diabetes-associated miRNAs to modulate endothelial function, inflammaging and cellular senescence. We also discuss the hypothesis that miRNA-containing extracellular vesicles (i.e. exosomes and microvesicles) could be harnessed to restore a 'physiological' signature capable of preventing or delaying the harmful systemic effects of T2DM. Type 2 diabetes mellitus (T2DM) is a major cause of cardiovascular (CV) disease. Several large clinical trials have shown that the risk for patients with diabetes of developing CV complications is only partially reduced by early, intensive glycaemic control and lifestyle interventions, and that such complications result from changes in complex, not fully explored networks that contribute to the maintenance of endothelial function. The accumulation of senescent cells and the low-grade, systemic, inflammatory status that accompanies aging (inflammaging) are involved in the development of endothelial dysfunction. Such phenomena are modulated by epigenetic mechanisms, including microRNAs (miRNAs). MiRNAs can modulate virtually all gene transcripts. They can be secreted by living cells and taken up in active form by recipient cells, providing a new communication tool between tissues and organs. MiRNA deregulation has been associated with the development and progression of a number of age-related diseases, including the enduring gene expression changes seen in patients with diabetes. We review recent evidence on miRNA changes in T2DM, focusing on the ability of diabetes-associated miRNAs to modulate endothelial function, inflammaging and cellular senescence. We also discuss the hypothesis that miRNA-containing extracellular vesicles (i.e. exosomes and microvesicles) could be harnessed to restore a 'physiological' signature capable of preventing or delaying the harmful systemic effects of T2DM.Type 2 diabetes mellitus (T2DM) is a major cause of cardiovascular (CV) disease. Several large clinical trials have shown that the risk for patients with diabetes of developing CV complications is only partially reduced by early, intensive glycaemic control and lifestyle interventions, and that such complications result from changes in complex, not fully explored networks that contribute to the maintenance of endothelial function. The accumulation of senescent cells and the low-grade, systemic, inflammatory status that accompanies aging (inflammaging) are involved in the development of endothelial dysfunction. Such phenomena are modulated by epigenetic mechanisms, including microRNAs (miRNAs). MiRNAs can modulate virtually all gene transcripts. They can be secreted by living cells and taken up in active form by recipient cells, providing a new communication tool between tissues and organs. MiRNA deregulation has been associated with the development and progression of a number of age-related diseases, including the enduring gene expression changes seen in patients with diabetes. We review recent evidence on miRNA changes in T2DM, focusing on the ability of diabetes-associated miRNAs to modulate endothelial function, inflammaging and cellular senescence. We also discuss the hypothesis that miRNA-containing extracellular vesicles (i.e. exosomes and microvesicles) could be harnessed to restore a 'physiological' signature capable of preventing or delaying the harmful systemic effects of T2DM. |
| Author | Procopio, A. D. Genovese, S. Olivieri, F. Ceriello, A. Prattichizzo, F. Giuliani, A. De Nigris, V. Testa, R. Pujadas, G. Ceka, A. La Sala, L. |
| AuthorAffiliation | 4 Experimental Models in Clinical Pathology INRCA‐IRCCS National Institute Ancona Italy 1 Insititut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) Barcelona Spain 5 Center of Clinical Pathology and Innovative Therapy, INRCA‐IRCCS National Institute Ancona Italy 3 Department of Cardiovascular and Metabolic Diseases IRCCS Gruppo Multimedica Milan Italy 2 Department of Clinical and Molecular Sciences, DISCLIMO Università Politecnica delle Marche Ancona Italy |
| AuthorAffiliation_xml | – name: 1 Insititut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM) Barcelona Spain – name: 5 Center of Clinical Pathology and Innovative Therapy, INRCA‐IRCCS National Institute Ancona Italy – name: 4 Experimental Models in Clinical Pathology INRCA‐IRCCS National Institute Ancona Italy – name: 3 Department of Cardiovascular and Metabolic Diseases IRCCS Gruppo Multimedica Milan Italy – name: 2 Department of Clinical and Molecular Sciences, DISCLIMO Università Politecnica delle Marche Ancona Italy |
| Author_xml | – sequence: 1 givenname: F. surname: Prattichizzo fullname: Prattichizzo, F. email: : Francesco Prattichizzo, PhD, Insititut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), C/Rosselló, 149-153, 08036, Barcelona, Spain., f.prattichizzo@univpm.it organization: Insititut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain – sequence: 2 givenname: A. surname: Giuliani fullname: Giuliani, A. organization: Department of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy – sequence: 3 givenname: V. surname: De Nigris fullname: De Nigris, V. organization: Insititut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain – sequence: 4 givenname: G. surname: Pujadas fullname: Pujadas, G. organization: Insititut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain – sequence: 5 givenname: A. surname: Ceka fullname: Ceka, A. organization: Department of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy – sequence: 6 givenname: L. surname: La Sala fullname: La Sala, L. organization: Department of Cardiovascular and Metabolic Diseases, IRCCS Gruppo Multimedica, Milan, Italy – sequence: 7 givenname: S. surname: Genovese fullname: Genovese, S. organization: Department of Cardiovascular and Metabolic Diseases, IRCCS Gruppo Multimedica, Milan, Italy – sequence: 8 givenname: R. surname: Testa fullname: Testa, R. organization: Experimental Models in Clinical Pathology, INRCA-IRCCS National Institute, Ancona, Italy – sequence: 9 givenname: A. D. surname: Procopio fullname: Procopio, A. D. organization: Department of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy – sequence: 10 givenname: F. surname: Olivieri fullname: Olivieri, F. organization: Department of Clinical and Molecular Sciences, DISCLIMO, Università Politecnica delle Marche, Ancona, Italy – sequence: 11 givenname: A. surname: Ceriello fullname: Ceriello, A. organization: Insititut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS) and Centro de Investigación Biomédica en Red de Diabetes y Enfermedades Metabólicas Asociadas (CIBERDEM), Barcelona, Spain |
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| Copyright | 2016 The Authors. Diabetes, Obesity and Metabolism published by John Wiley & Sons Ltd. 2016 John Wiley & Sons Ltd 2016. This article is published under http://creativecommons.org/licenses/by-nc/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| PublicationTitleAlternate | Diabetes Obes Metab |
| PublicationYear | 2016 |
| Publisher | Blackwell Publishing Ltd Wiley Subscription Services, Inc |
| Publisher_xml | – name: Blackwell Publishing Ltd – name: Wiley Subscription Services, Inc |
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| SubjectTerms | Aging Aging - metabolism antidiabetic drug Antidiabetics cardiovascular disease Cell interactions Cellular Senescence Clinical trials Diabetes diabetes complications Diabetes mellitus (non-insulin dependent) Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - metabolism Diabetic Angiopathies - metabolism Diabetic Angiopathies - physiopathology Endothelium, Vascular - metabolism Endothelium, Vascular - physiopathology Epigenesis, Genetic Epigenetics Exosomes extracellular vesicles Extracellular Vesicles - metabolism extracellular vesicles, exosomes Gene expression glycaemic control Humans Hyperglycemia - metabolism Hypoglycemic Agents - therapeutic use Inflammation metabolic memory metformin MicroRNAs MicroRNAs - metabolism miRNA Review Senescence type 2 diabetes |
| Title | Extracellular microRNAs and endothelial hyperglycaemic memory: a therapeutic opportunity? |
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