Abstract
Myocardial cellular and extracellular matrix remodeling are important in the development of left ventricular hypertrophy and are essential for the adaptive and maladaptive changes associated with the cardiometabolic syndrome. This brief review of myocyte remodeling also presents preliminary observational findings regarding myocardial adaptive hypertrophy remodeling, including an increase in mitochondria and capillaries, convolutions and lengthening of intercalated discs, the addition of sarcomeres, thickened Z lines, and the novel presence of pericapillary fibrosis (in addition to perivascular arteriolar fibrosis). The 11-week-old TG(mREN-2)27 transgene rat model of tissue angiotensin II overexpression, which develops hypertension and insulin resistance, was chosen to examine both myocyte hypertrophy and extracellular matrix fibrosis. This review and the preliminary observational findings may provide the clinician and researcher a better understanding of remodeling changes in the myocardium and ultimately foster earlier recognition and therapeutic interventions.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, U.S. Gov't, Non-P.H.S.
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Review
MeSH terms
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Albuminuria / pathology
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Albuminuria / physiopathology
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Animals
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Animals, Genetically Modified
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Cardiomyopathies / etiology
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Cardiomyopathies / pathology
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Cardiomyopathies / physiopathology
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Cardiovascular Diseases / etiology*
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Cardiovascular Diseases / metabolism
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Cardiovascular Diseases / pathology
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Cardiovascular Diseases / physiopathology
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Disease Models, Animal
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Extracellular Matrix / metabolism
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Fibrosis
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Glucose Intolerance / pathology
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Glucose Intolerance / physiopathology
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Humans
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Hyperinsulinism / pathology
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Hyperinsulinism / physiopathology
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Hypertension / pathology
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Hypertension / physiopathology
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Hypertrophy
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Metabolic Syndrome / complications
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Metabolic Syndrome / metabolism
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Metabolic Syndrome / pathology
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Metabolic Syndrome / physiopathology*
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Mice
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Myocytes, Cardiac / metabolism
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Myocytes, Cardiac / pathology*
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Obesity / pathology
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Obesity / physiopathology
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Oxidative Stress
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Rats
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Renin / genetics
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Renin / metabolism
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Ventricular Remodeling*
Substances
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Ren2 protein, mouse
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Renin