Vascular autophagy and endothelial cell nitric oxide generation

Symposium — Monday, April 24, 2024 — 8:00 AM - 10:00 AM — , Room W196B
Cardiovascular Section — Chair: J David Symons — Co-Chair: David Gutterman

Healthy aging and pathophysiological conditions (e.g., obesity, insulin-resistance, type 2 diabetes) can precipitate macrovascular and microvascular complications. Common among both pathologies is endothelial dysfunction. Endothelial dysfunction is characterized by decreased production of nitric oxide (NO) by endothelial NO synthase (eNOS), a key regulator of blood pressure, arterial stiffness, adhesion, permeability, inflammation, and vasomotion. The precise molecular mechanisms responsible for impaired eNOS activity in the context of healthy aging and pathophysiological conditions remain elusive. Obtaining new knowledge in this area is critical so that novel therapeutic targets of intervention can be identified in an effort to alleviate personal suffering and cost, and costs to society. Targeting the metabolism of endothelial cells in general, and the process of autophagy in particular, is a novel and emerging strategy. This symposium will provide current information concerning the contribution from vascular autophagy to endothelial cell NO generation in physiological and pathophysiological situations, from cells to systems, using pre-clinical models and humans.

Speakers

• Autophagy maintains vascular function through a novel glycolysis-linked pathway regulating eNOS
  Leena P Bharath — Microbiology, Boston University


• Regulation of vascular smooth muscle cell migration by autophagy
  Ming Hui Zou — Center for Molecular and Translational Medicine, Georgia State University


• Autophagy is a novel regulatory mechanism in the human microcirculation
  Andreas M. Beyer — Medicine and Physiology, Medical College of Wisconsin


• Autophagy, aging, and arterial function
  Thomas LaRocca — Integrative Physiology, University of Colorado Boulder