The DOI matches its Crossref record; 173 of the 173 references it cites were found in a registry or an index.
Rodent models of diabetic cardiomyopathy
Abstract
Diabetic cardiomyopathy increases the risk of heart failure in individuals with diabetes, independently of co-existing coronary artery disease and hypertension. The underlying mechanisms for this cardiac complication are incompletely understood. Research on rodent models of type 1 and type 2 diabetes, and the use of genetic engineering techniques in mice, have greatly advanced our understanding of the molecular mechanisms responsible for human diabetic cardiomyopathy. The adaptation of experimental techniques for the investigation of cardiac physiology in mice now allows comprehensive characterization of these models. The focus of the present review will be to discuss selected rodent models that have proven to be useful in studying the underlying mechanisms of human diabetic cardiomyopathy, and to provide an overview of the characteristics of these models for the growing number of investigators who seek to understand the pathology of diabetes-related heart disease.
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Cites
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Mechanisms of Diabetic Complications
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Molecular mechanisms of diabetic cardiomyopathy
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Self-citationBasic Mechanisms of Diabetic Heart Disease
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Implications of Underlying Mechanisms for the Recognition and Management of Diabetic Cardiomyopathy
Marwick, T. H., Ritchie, R., Shaw, J. E., & Kaye, D. (2018) · Journal of the American College of Cardiology · doi:10.1016/j.jacc.2017.11.019 · Cited by 365
Metadata
- Authors
- Bugger, H., & Abel, E. D.
- Venue
- Disease Models & Mechanisms
- Publisher
- The Company of Biologists
- Published
- 2009-09-02
- Volume
- 2
- Issue
- 9-10
- Pages
- 454-466
- ISSN
- 1754-8403 (ISSN-L)
- 1754-8411
- OpenAlex
- W2149067762
- Cited by
- 285
- References
- 173
- FWCI
- 9.89
- Type
- journal article
- Language
- en
- Open access
- closed
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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