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Hypertension. 2004;43:693-698
Published online before print February 16, 2004, doi: 10.1161/01.HYP.0000120963.09029.ca
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(Hypertension. 2004;43:693.)
© 2004 American Heart Association, Inc.

Brief Reviews

Angiotensin II and Cell Cycle Regulation

Gunter Wolf; Ulrich O. Wenzel

From the Department of Medicine, Division of Nephrology and Osteology, University of Hamburg, Germany.

Correspondence to Dr Gunter Wolf, University of Hamburg, University Hospital, Eppendorf Department of Medicine, Division of Nephrology and Osteology, Pavilion N26, Martinistraße 52 D-20246, Hamburg, Germany. E-mail Wolf{at}UKE.uni-hamburg.de

Angiotensin II has emerged as an important growth factor for vascular, cardiac, and renal cells. Depending on the specific cell type and presence of other growth factors, angiotensin II induces proliferation (replication of DNA with subsequent successful division of cells), hypertrophy (increase in cell size, cell protein, and mRNA content without DNA replication), apoptosis (programmed cell death), or differentiation. Such angiotensin II-mediated modulation of growth process may underlie various pathophysiological processes such as atherosclerosis, vascular and cardiac remodeling, and progression of chronic renal disease. Clearly, angiotensin II-induced proliferation requires complete cell progression through the various steps of the cell cycle. In contrast, cells undergoing angiotensin II-mediated hypertrophy are arrested in the G1-phase. Upregulation of cell cycle-dependent kinase inhibitors (eg, p27Kip1) plays an important role in this process. Although accumulating evidence suggests that apoptosis is cell cycle-dependent, only few data are currently available concerning the interaction of angiotensin II with the cell cycle machinery in apoptosis. We review the various angiotensin II-mediated growth processes and their relationship to events governing cell cycle regulation.


Key Words: renin-angiotensin system • hypertrophy • apoptosis




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