Abstract
Over the past millennium, great strides have been made in expanding the human life span. Such gains however, have come with the cost of increasing age-related diseases such as Alzheimer’s disease. Slowing “biological” aging therefore may be a way to reduce morbidity and significantly impact the quality of life for the elderly. Enhanced angiotensin II (Ang II) signal transduction has been implicated in premature aging and evidence exists for the prolongation of life through blockade of the Ang II type-1 receptor (AT1R). In this Viewpoint article, we will discuss noteworthy similarities between Ang II pathophysiology and Alzheimer’s disease as potential intervention points to promote healthy aging.
Keywords:
aging; autophagy; blood pressure; mitochondria; senescence.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
MeSH terms
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Age Factors
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Aging / drug effects
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Aging / metabolism*
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Aging / pathology
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Alzheimer Disease / drug therapy
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Alzheimer Disease / metabolism*
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Alzheimer Disease / pathology
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Alzheimer Disease / physiopathology
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Angiotensin II / metabolism*
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Angiotensin II Type 1 Receptor Blockers / therapeutic use
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Angiotensin-Converting Enzyme Inhibitors / therapeutic use
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Animals
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Autophagy
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Brain / drug effects
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Brain / metabolism*
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Brain / pathology
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Brain / physiopathology
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Cardiovascular Diseases / drug therapy
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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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Cardiovascular System / drug effects
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Cardiovascular System / metabolism*
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Cardiovascular System / pathology
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Cardiovascular System / physiopathology
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Cellular Senescence
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Humans
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Receptor, Angiotensin, Type 1 / metabolism
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Renin-Angiotensin System* / drug effects
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Signal Transduction
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Unfolded Protein Response
Substances
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AGTR1 protein, human
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Angiotensin II Type 1 Receptor Blockers
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Angiotensin-Converting Enzyme Inhibitors
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Receptor, Angiotensin, Type 1
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Angiotensin II