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JOHN S. TORDAY:
My name is John Torday.
I'm a professor of evolutionary
medicine at UCLA.
This is lecture 15 in
the evolutionary physiology lecture
series entitled, "Using
Lung Evolution as a Cipher
for Physiology and Pathophysiology."
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The premise of the evolutionary
approach to physiology
and pathophysiology alike is that
the unicellular interrelationships
that mediate structure
and function are part
of the history of
cell-cell communications
that coincide with
ontogeny and phylogeny.
From this perspective,
the lung is the best understood
complex physiologic
mechanism, so it will
be used as a cipher to understand
physiology and pathophysiology
as a continuum, rather than
as the dogmatic associations
and correlations of conventional
descriptive physiology
and the dichotomous
perspective on disease
as the absence of
health, which still
prevails in the era of genomics,
proteomics, metabolomics, etc.
Shown in this schematic is
the role of the lipofibroblast
in homeostatic regulation
of lung surfactant,
mediating the recruitment
of neutral lipid substrate
from the microcirculation for
the on-demand production of surfactant,
preventing alveolar collapse
due to elevated surface
tension on expansion of
the lung for gas exchange.
Damage by a wide variety
of agents, ranging
from pressure, or
barotrauma, to oxygen,
or oxotrauma, infection,
and prematurity,
all funneling through
the mechanism of lipfibroblast injury
in which loss of cell-cell
communication with the alveolar
type II cell causes
transdifferentiation of
the lipofibroblast to a myofibroblast.
A myofibroblast is the final
common pathway for all chronic lung
diseases, including
Brocopulmonary Dysplasia, or BPD,
a chronic lung disease
caused by lung immaturity.
