Key result
A review of published results indicates no evidence that angiotensin II directly triggers mitogenesis through the cyclin-dependent pathway in cardiac fibroblasts.
Why the study?
Does angiotensin II directly stimulate proliferation in cardiac fibroblasts?
Does angiotensin II directly stimulate proliferation in cardiac fibroblasts?
Angiotensin II likely promotes cardiac fibroblast proliferation indirectly by stimulating the synthesis of growth factors and cytokines rather than through direct mitogenesis.
No direct cyclin-dependent mitogenesis by angiotensin II in fibroblasts; leaves open indirect growth factor mechanisms for targeted study.
Angiotensin II has been implicated as an important factor in cardiac remodeling, particularly in the development of pathological left ventricular hypertrophy. It is generally assumed that angiotensin II is able to alter the phenotype of cardiac myocytes and fibroblasts, and several experiments have suggested that this peptide can particularly affect the proliferation of cardiac fibroblasts. However, a review of the published results indicates that there is no evidence that angiotensin II can directly trigger mitogenesis through activation of the cyclin-dependent pathway. The observed proliferative effect might well be caused by stimulation of the synthesis of growth or inflammatory substances like platelet-derived growth factor and cytokines, by integrin activation due to secreted extracellular matrix proteins, or by a combination of these mechanisms. Angiotensin II thus appears to differentiate cardiac fibroblasts into a growth substance-secreting phenotype.
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F Bouzegrhane (2002) conducted a review in Cardiac remodeling and left ventricular hypertrophy. Angiotensin II was evaluated on Mitogenesis and proliferation of cardiac fibroblasts. A review of published results indicates no evidence that angiotensin II directly triggers mitogenesis through the cyclin-dependent pathway in cardiac fibroblasts.
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