Abstract
If somatic angiotensin I-converting enzyme (ACE) were a mechanosensor, as recently claimed, it would provide insight into the molecular origin of most adult diseases, such as diabetes, cancer, autoimmune diseases, and psychiatric disease, as well as aging itself. The "ACE as mechanosensor" hypothesis holds that tissue ACE is activated by turbulent flow with each heart beat, so that age-dependent diseases begin with a signal from the vasculature. Activation of ACE would thus represent the first of many amplification steps ("cascades"), placing it at the origin of most age-dependent diseases. As a corollary, effective inhibition of tissue ACE might significantly delay the progression of most diseases of aging. In this paper we will explore how useful this hypothesis is in explaining the molecular pathogenesis of diabetes and its complications, in which aging is accelerated.
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