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Using lung evolution as a cipher for physiology - pathophysiology

Published on March 31, 2016   18 min

A selection of talks on Clinical Practice

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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.
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