Molecular mechanisms of diabetic cardiomyopathy

Bugger, Heiko; Abel, E. Dale

doi:10.1007/s00125-014-3171-6

Cited by 905Cardiovascular Function and Risk FactorsCardiac Fibrosis and RemodelingCardiomyopathy and Myosin Studies

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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Maternal diabetes increases cardiac fibrosis in the offspring.
“Maternal diabetes also increased cardiomyocyte size and cardiac fibrosis in the offspring [119].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [119]
The Fibrosis section reports increased fibrosis in people and rodents with diabetes, but does not discuss maternal diabetes or fibrosis in offspring. Searches for maternal diabetes, offspring, and cardiomyocyte size found no passage addressing that specific claim; the copy is not marked as truncated. (LLM, conf=0.70)
Experimental — accuracy not yet measured
Maternal diabetes increases cardiomyocyte size in the offspring.
“Maternal diabetes also increased cardiomyocyte size and cardiac fibrosis in the offspring [119].”
From Recent Experimental Studies of Maternal Obesity, Diabetes during Pregnancy and the Developmental Origins of Cardiovascular Disease (2022) · cites this paper as [119]
The Structural and functional changes section describes cardiac hypertrophy in people with diabetes, and the Fibrosis section describes fibrosis in diabetic hearts. Neither addresses cardiomyocyte size or cardiac fibrosis in offspring exposed to maternal diabetes; searches for maternal diabetes and offspring found no passage on that point. (LLM, conf=0.76)
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2 retracted

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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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Sex and Gender Differences in Risk, Pathophysiology and Complications of Type 2 Diabetes Mellitus
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Heart Failure: An Underappreciated Complication of Diabetes. A Consensus Report of the American Diabetes Association
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Targeting mitochondrial dynamics by regulating Mfn2 for therapeutic intervention in diabetic cardiomyopathy
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Mitochondrial Structure and Function in Human Heart Failure
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Sodium–glucose cotransporter 2 inhibitor Dapagliflozin attenuates diabetic cardiomyopathy
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lncRNA H19/miR-675 axis regulates cardiomyocyte apoptosis by targeting VDAC1 in diabetic cardiomyopathy
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lncRNA MIAT functions as a competing endogenous RNA to upregulate DAPK2 by sponging miR-22-3p in diabetic cardiomyopathy
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Direct Cardiac Actions of Sodium Glucose Cotransporter 2 Inhibitors Target Pathogenic Mechanisms Underlying Heart Failure in Diabetic Patients
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Diabetic Cardiomyopathy: Does the Type of Diabetes Matter?
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Mitochondrial Mechanisms in Septic Cardiomyopathy
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CTRP3 attenuates cardiac dysfunction, inflammation, oxidative stress and cell death in diabetic cardiomyopathy in rats
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The role of SIRT1 in diabetic cardiomyopathy
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Upregulation of MG53 Induces Diabetic Cardiomyopathy Through Transcriptional Activation of Peroxisome Proliferation-Activated Receptor α
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MD2 activation by direct AGE interaction drives inflammatory diabetic cardiomyopathy
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USP28 Serves as a Key Suppressor of Mitochondrial Morphofunctional Defects and Cardiac Dysfunction in the Diabetic Heart
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Regulated cell death pathways in cardiomyopathy
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Inhibition of fatty acid uptake by TGR5 prevents diabetic cardiomyopathy
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Empagliflozin Attenuates Myocardial Sodium and Calcium Dysregulation and Reverses Cardiac Remodeling in Streptozotocin-Induced Diabetic Rats
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Autophagy Inhibition Enables Nrf2 to Exaggerate the Progression of Diabetic Cardiomyopathy in Mice
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Mesenchymal stem cells promote type 2 macrophage polarization to ameliorate the myocardial injury caused by diabetic cardiomyopathy
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LncRNA HOTAIR functions as a competing endogenous RNA to upregulate SIRT1 by sponging miR‐34a in diabetic cardiomyopathy
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Self-citation

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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