UNIVERSITY SCHOLAR SEMINAR
Presented by
Russell P. Tracy, PhD
Professor of Pathology and Biochemistry
Director, Laboratory for Clinical Biochemistry Research
Professor of Pathology and Biochemistry
Director, Laboratory for Clinical Biochemistry Research
Inflammation, Atherosclerosis and Aging: the Inflammation Hypothesis of Aging
“…inflammation of the inner arterial coat [is] the starting point of the so-called atheromatous degeneration.”
R. Virchow, 1859.
“Longevity
is a vascular question, which has been well expressed in the axiom ‘a
man is as old as his arteries.’ To a majority of men, death comes
primarily or secondarily through this portal.” William Osler, 1892.
“Yep, son, we have met the enemy and he is us!” Pogo to Porky (as written by
Walt Kelly), 1971
Over the last 15 years we have come to
understand that the human inflammatory response is a major part of
atherosclerosis, the pathophysiological process that leads to most of
the heart disease in the world. This position was held by some in the
past, but not well understood by most researchers and practitioners in
the field until recently. Additionally, we have come to understand that
inflammation as a response to a variety of stressors is part of not
only atherosclerosis, but many (all?) of the chronic diseases
associated with aging, such as insulin
resistance, osteoporosis, dementia and others. Our laboratory has
contributed to this work through molecular, cellular, and genetic
epidemiology in a variety of fields.
Because of this work, some of which we will
discuss in this talk, we and others recently have proposed a broad
concept, an “inflammation hypothesis of aging”. This hypothesis
suggests that the cumulative lifetime burden of our own inflammatory
responses, while critically important to short-term survival, plays a
major role in the aging process itself.
Within this conceptual framework, we propose
that the time-dependent inflammation-driven deterioration of individual
organ function has multi-organ system-wide consequences, which
ultimately yield an exponential decline in health (i.e., frailty and
death). This decline starts at an age which appears to be at least in
part driven by evolutionary biology and natural selection. We also
propose that the rate of decline in any individual is a function of the
environmental stresses to which she/he must respond, and the degree of
response which is in turn driven by genetic architecture and
physiological response capacity. Finally, we propose that within this
framework, many diseases can be viewed as organ-specific accelerated
aging with systemic ramifications. If validated, this view has
implications for a broad range of translational research issues from
pharmaceutical development to diagnostic biomarkers and the
interpretation of high resolution biomedical imaging.
4:00 PM, Thursday, October 22, 2009
Memorial Lounge, Waterman Building
The
University Scholar Awards Program annually recognizes distinguished faculty members for sustained excellence
in research and scholarly activities. The Scholars are selected by a panel of distinguished faculty, based upon nominations submitted by UVM colleagues.
Refreshments at 3:45 and after the Seminar
Sponsored by the Graduate College
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