The Pathogenesis of Myocardial Fibrosis in the Setting of Diabetic Cardiomyopathy
Author + information
- Received May 19, 2005
- Revision received August 24, 2005
- Accepted September 26, 2005
- Published online February 21, 2006.
Author Information
- ↵⁎Reprint requests and correspondence:
Dr. Francisco J. Villarreal, UCSD, 9500 Gilman Drive, La Jolla, California 92093-0613J.
Abstract
Diabetes has emerged as a major threat to worldwide health. The increasing incidence of diabetes in young individuals is particularly worrisome given that the disease is likely to evolve over a period of years. In 1972, the existence of a diabetic cardiomyopathy was proposed based on the experience with four adult diabetic patients who suffered from congestive heart failure in the absence of discernible coronary artery disease, valvular or congenital heart disease, hypertension, or alcoholism. The exact mechanisms underlying the disease are unknown; however, an important component of the pathological alterations observed in these hearts includes the accumulation of extracellular matrix (ECM) proteins, in particular collagens. The excess deposition of ECM in the heart mirrors what occurs in other organs such as the kidney and peritoneum of diabetics. Mechanisms responsible for these alterations may include the excess production, reduced degradation, and/or chemical modification of ECM proteins. These effects may be the result of direct or indirect actions of high glucose concentrations. This article reviews our state of knowledge on the effects that diabetes-like conditions exert on the cells responsible for ECM production as well as relevant experimental and clinical data.
Footnotes
Joel Karliner acted as the Guest Editor for this review.
- Received May 19, 2005.
- Revision received August 24, 2005.
- Accepted September 26, 2005.
- American College of Cardiology Foundation
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Article Outline
- Top
- Abstract
- Organ fibrosis as a pathological observation of longstanding diabetes
- Fibrosis in the human diabetic heart
- Animal models of diabetic cardiomyopathy
- The effects of pharmacotherapy
- In vitro models of diabetes
- Paracrine and mechanical factors
- Reactive oxygen species
- Signaling
- Concluding remarks
- Footnotes
- References