Proposing a Microvascular Theory of Aging

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It seems that everyone has their own theory of aging these days, something that might be taken as a sign of increased interest in the field:

One of the main features of human aging is the loss of adult stem cell homeostasis. Organs that are very dependent on adult stem cells show increased susceptibility to aging, particularly organs that present a vascular stem cell niche. Reduced regenerative capacity in tissues correlates with reduced stem cell function, which parallels a loss of microvascular density (rarefraction) and plasticity. Moreover, the age-related loss of microvascular plasticity and rarefaction has significance beyond metabolic support for tissues because stem cell niches are regulated co-ordinately with the vascular cells. In addition, microvascular rarefaction is related to increased inflammatory signals that may negatively regulate the stem cell population. Thus, the processes of microvascular rarefaction, adult stem cell dysfunction, and inflammation underlie the cycle of physiological decline that we call aging.
Observations from new mouse models and humans are discussed here to support the vascular aging theory. We develop a novel theory to explain the complexity of aging in mammals and perhaps in other organisms. The connection between vascular endothelial tissue and organismal aging provides a potential evolutionary conserved mechanism that is an ideal target for the development of therapies to prevent or delay age-related processes in humans.

Link: http://online.liebertpub.com/doi/full/10.1089/rej.2013.1440

Comments

heh - here's an email from me to GRG from 09:38 AM 8/6/2010, you wrote:
Another approach might be peripheral vs. core blood pressure -- (ankle/brachial)
differential over time in asymptomatic/non-diabetic/non-smokers?

The hypothesis is that the smallest vascular tributaries would die back first and proceed
progressively toward the center at a statistically-predictable rate. As the rivers die, so dies
the land.
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Geriatric devascularization, blood vessel die back:

Loss of vascularization
Fragile cells
Slow repair recovery
Misrecognition by immune system
Autoimune pathology
Accelerated tissue apoptosis decay, decline
Clinical chronic inflammation
Slow healing, loss of function, macro-clinical insults
Death

Methuselah is pursuing/sponsoring the NewOrgan Liver prize in part to bring about engineering solutions to creating and/or restoring our microvasculature.

Cheers,
Dave
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Posted by: Dave at December 23rd, 2013 4:13 PM

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