Cited by 903Cardiovascular Function and Risk FactorsCardiac Fibrosis and RemodelingCardiomyopathy and Myosin Studies

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Molecular mechanisms of diabetic cardiomyopathy

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Bugger, Heiko, Abel, E. Dale·2014·Diabetologia

DOI 10.1007/s00125-014-3171-6PMC PMC3969857

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Abstract

In recent years, diabetes mellitus has become an epidemic and now represents one of the most prevalent disorders. Cardiovascular complications are the major cause of mortality and morbidity in diabetic patients. While ischaemic events dominate the cardiac complications of diabetes, it is widely recognised that the risk for developing heart failure is also increased in the absence of overt myocardial ischaemia and hypertension or is accelerated in the presence of these comorbidities. These diabetes-associated changes in myocardial structure and function have been called diabetic cardiomyopathy. Numerous molecular mechanisms have been proposed to contribute to the development of diabetic cardiomyopathy following analysis of various animal models of type 1 or type 2 diabetes and in genetically modified mouse models. The steady increase in reports presenting novel mechanistic data on this subject expands the list of potential underlying mechanisms. The current review provides an update on molecular alterations that may contribute to the structural and functional alterations in the diabetic heart.

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MicroRNA miR-133 Represses HERG K+ Channel Expression Contributing to QT Prolongation in Diabetic Hearts
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Retracted
Retracted: Advanced glycation endproduct (AGE) accumulation and AGE receptor (RAGE) up‐regulation contribute to the onset of diabetic cardiomyopathy
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Most mammalian mRNAs are conserved targets of microRNAs
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Retracted
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Authors: Bugger, H., & Abel, E. D.
Affiliations: University of Freiburg (DE)
University of Iowa (US)
Corresponding author: Abel, E. Dale
ORCID: Bugger, Heiko
Abel, E. Dale
Venue: Diabetologia
Publisher: Springer Science and Business Media LLC
Published: 2014-01-30
Volume: 57
Issue: 4
Pages: 660-671
ISSN: 0012-186X (ISSN-L)
1432-0428
DOI: 10.1007/s00125-014-3171-6
PMC: PMC3969857
OpenAlex: W2006499762
Cited by: 903
References: 153
Citations by year: 2026: 51 · 2025: 76 · 2024: 75 · 2023: 79 · 2022: 95 · 2021: 103 · 2020: 100 · 2019: 66 · 2018: 84 · 2017: 62 · 2016: 54 · 2015: 43 · 2014: 14
FWCI: 9.29
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springer.com/tdm (tdm)
Locations: Diabetologia (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Heart, Lung, and Blood Institute (R01HL108379, U01HL087947)
National Institute of Diabetes and Digestive and Kidney Diseases (R01DK092065)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiomyopathy and Myosin Studies
Keywords: diabetic cardiomyopathy, diabetes mellitus, heart failure, myocardial structure and function, type 1 diabetes, type 2 diabetes, animal models of diabetes, genetically engineered mouse models, cardiovascular complications of diabetes
MeSH terms: Animals, Diabetes Mellitus, Type 1, Diabetes Mellitus, Type 2, Heart Failure, Humans, Diabetic Cardiomyopathies

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