Key result
ACE inhibitors and angiotensin receptor antagonists may influence disease progression through direct inhibition of angiotensin-induced apoptosis, offering potential novel uses in controlling cell death.
Why the study?
Do ACE inhibitors and angiotensin receptor antagonists inhibit ANG-induced apoptosis in cardiovascular disease models?
Do ACE inhibitors and angiotensin receptor antagonists inhibit ANG-induced apoptosis in cardiovascular disease models?
This review highlights the potential of ACE inhibitors and angiotensin receptor antagonists to influence cardiovascular disease progression by directly inhibiting apoptosis.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating only; leaves open whether apoptosis effects alter cardiovascular outcomes.
Inhibitors of angiotensin converting enzyme (ACE-Is) and angiotensin (ANG) receptor antagonists were originally developed to aid in the management of hypertension. As the use of these agents was extended to the management of heart failure and other cardiovascular diseases, studies of tissue remodeling suggested that blockade of ANGII function might play a role in the regulation of cell death by apoptosis. Experiments with cultured cells confirmed that ANGII is an inducer of apoptosis in well differentiated cell types isolated from the heart, kidneys, lungs and other organs. More recent evidence with animal models strongly suggests that ACE-Is and ANG receptor antagonists, in addition to affecting hemodynamics, also influence disease progression through direct inhibition of ANG-induced apoptosis. This manuscript reviews the evidence supporting this view, discusses its potential relevance to disease pathogenesis and offers new hypotheses regarding novel uses of ACE-Is and ANG receptor antagonists in the control of cell death.
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Filippatos et al. (2003) conducted a review in Cardiovascular diseases. ACE Inhibitors and Angiotensin Receptor Antagonists was evaluated. ACE inhibitors and angiotensin receptor antagonists may influence disease progression through direct inhibition of angiotensin-induced apoptosis, offering potential novel uses in controlling cell death.
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