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Reactive oxygen species and vascular cell apoptosis in response to angiotensin II and pro-atherosclerotic factors.
Regul Pept 2000; 90(1-3):19-25RP

Abstract

Reactive oxygen species (ROS) are known to induce apoptotic cell death in various cell types. In the vessel wall, ROS can be formed by macrophages within the atherosclerotic plaque or can act on the endothelium after adhesion of monocytes or leucocytes. Moreover, ROS are endogenously synthesized by endothelial and vascular smooth muscle cells by NAD(P)H oxidase. Enhanced ROS production is a very early hallmark in the atherogenic process, suggesting a link between ROS and apoptosis. In endothelial cells, the endogenous generation of ROS is induced by different pro-inflammatory and pro-atherosclerotic factors such as Ang II, oxLDL or TNFalpha, which all promote the execution of programmed cell death. ROS synthesis is thereby causally involved in apoptosis induction, because antioxidants prevent endothelial cell death. The pro-apoptotic effects of endogenous ROS in endothelial cells mechanistically seems to involve the disturbance of mitochondrial membrane permeability followed by cytochrome c release, which finally activates the executioner caspases. In contrast to the pro-apoptotic capacity of ROS in endothelial cells, in vascular smooth muscle cells emerging evidence suggests that endogenous ROS synthesis promotes cell proliferation and hypertrophy and does not affect cell survival. However, high concentrations of exogenous ROS can also stimulate smooth muscle cell apoptosis as shown for other cell types probably via activation of p53. Taken together, the double-edged effects of endogenously derived ROS in endothelial cells versus VSMC may provide a mechanistic clue to the anti-atherosclerotic effects of antioxidants shown in experimental studies, given that the promotion of endothelial survival in combination with inhibition of VSMC proliferation blocks two very important steps in the pathogenesis of atherosclerosis.

Authors+Show Affiliations

Molecular Cardiology, Department of Internal Medicine IV, University of Frankfurt, Theodor-Stern-Kai 7, 60590, Frankfurt, Germany. dimmeler@em.uni-frankfurt.deNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Review

Language

eng

PubMed ID

10828488

Citation

Dimmeler, S, and A M. Zeiher. "Reactive Oxygen Species and Vascular Cell Apoptosis in Response to Angiotensin II and Pro-atherosclerotic Factors." Regulatory Peptides, vol. 90, no. 1-3, 2000, pp. 19-25.
Dimmeler S, Zeiher AM. Reactive oxygen species and vascular cell apoptosis in response to angiotensin II and pro-atherosclerotic factors. Regul Pept. 2000;90(1-3):19-25.
Dimmeler, S., & Zeiher, A. M. (2000). Reactive oxygen species and vascular cell apoptosis in response to angiotensin II and pro-atherosclerotic factors. Regulatory Peptides, 90(1-3), pp. 19-25.
Dimmeler S, Zeiher AM. Reactive Oxygen Species and Vascular Cell Apoptosis in Response to Angiotensin II and Pro-atherosclerotic Factors. Regul Pept. 2000 Jun 30;90(1-3):19-25. PubMed PMID: 10828488.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reactive oxygen species and vascular cell apoptosis in response to angiotensin II and pro-atherosclerotic factors. AU - Dimmeler,S, AU - Zeiher,A M, PY - 2000/6/1/pubmed PY - 2000/8/19/medline PY - 2000/6/1/entrez SP - 19 EP - 25 JF - Regulatory peptides JO - Regul. Pept. VL - 90 IS - 1-3 N2 - Reactive oxygen species (ROS) are known to induce apoptotic cell death in various cell types. In the vessel wall, ROS can be formed by macrophages within the atherosclerotic plaque or can act on the endothelium after adhesion of monocytes or leucocytes. Moreover, ROS are endogenously synthesized by endothelial and vascular smooth muscle cells by NAD(P)H oxidase. Enhanced ROS production is a very early hallmark in the atherogenic process, suggesting a link between ROS and apoptosis. In endothelial cells, the endogenous generation of ROS is induced by different pro-inflammatory and pro-atherosclerotic factors such as Ang II, oxLDL or TNFalpha, which all promote the execution of programmed cell death. ROS synthesis is thereby causally involved in apoptosis induction, because antioxidants prevent endothelial cell death. The pro-apoptotic effects of endogenous ROS in endothelial cells mechanistically seems to involve the disturbance of mitochondrial membrane permeability followed by cytochrome c release, which finally activates the executioner caspases. In contrast to the pro-apoptotic capacity of ROS in endothelial cells, in vascular smooth muscle cells emerging evidence suggests that endogenous ROS synthesis promotes cell proliferation and hypertrophy and does not affect cell survival. However, high concentrations of exogenous ROS can also stimulate smooth muscle cell apoptosis as shown for other cell types probably via activation of p53. Taken together, the double-edged effects of endogenously derived ROS in endothelial cells versus VSMC may provide a mechanistic clue to the anti-atherosclerotic effects of antioxidants shown in experimental studies, given that the promotion of endothelial survival in combination with inhibition of VSMC proliferation blocks two very important steps in the pathogenesis of atherosclerosis. SN - 0167-0115 UR - https://www.unboundmedicine.com/medline/citation/10828488/Reactive_oxygen_species_and_vascular_cell_apoptosis_in_response_to_angiotensin_II_and_pro_atherosclerotic_factors_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0167011500001051 DB - PRIME DP - Unbound Medicine ER -